<![CDATA[Newsroom University of Manchester]]> /about/news/ en Sun, 29 Dec 2024 13:01:54 +0100 Sun, 23 Apr 2023 17:40:38 +0200 <![CDATA[Newsroom University of Manchester]]> https://content.presspage.com/clients/150_1369.jpg /about/news/ 144 Manchester immunologist honoured for her public engagement work /about/news/manchester-immunologist--honoured-for-her-public-engagement-work/ /about/news/manchester-immunologist--honoured-for-her-public-engagement-work/570548Professor Sheena Cruickshank from Vlogٷ has been honoured  by the British Society for Immunology for her work raising awareness of the importance of immunology in our daily lives.

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Professor Sheena Cruickshank from Vlogٷ has been honoured  by the British Society for Immunology for her work raising awareness of the importance of immunology in our daily lives.

 

The , which recognises outstanding contributions to public engagement within immunology, was another feather in the immunologist cap.

 

She was one of 11 winners of the inaugural BSI Immunology Awards 2023, revealed at a special ceremony on Thursday 20 April

 

According to the BSI, Professor Cruickshank dedicated substantial time and effort to tackling misinformation during the COVID-19 pandemic

 

Her  public engagement activities include media appearances, social media activity, podcasts, citizen science, festivals, curating exhibitions and delivering public lectures.

Hear what she has has to say on this special video she recorded for the ceremony:

Some of her online articles accumulated over one million readers.

The awards was  open to nominations, and a shortlist was selected after careful review and deliberation by an expert , whose recommendation was then ratified by the BSI Nominations Committee.

The BSI Immunology Awards celebrate the remarkable achievements of individuals and teams shaping the future of immunology. We would like to congratulate all of the winners for this fantastic achievement.

Doug Brown, Chief Executive of the British Society for Immunology, said: “We are thrilled to recognise the achievements of these extraordinary individuals. Each of them dedicates their time and expertise to shaping the future of immunology, in many cases away from the limelight. Their efforts will ensure a brighter future for our field.

“Our heartfelt congratulations go to everyone who was shortlisted or nominated, and a huge thank you is due to our judges, those who nominated someone, the BSI Nominations Committee and everyone who was involved in making these awards a success. The response shows just how vibrant, supportive and talented the field of immunology is. Long may that continue.”

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Sun, 23 Apr 2023 16:40:38 +0100 https://content.presspage.com/uploads/1369/9c6d5b67-6199-4485-929f-98d2e3e5ddd8/500_sheenacruickshank3.jpg?10000 https://content.presspage.com/uploads/1369/9c6d5b67-6199-4485-929f-98d2e3e5ddd8/sheenacruickshank3.jpg?10000
People in urban areas have worse hay fever symptoms, analysis suggests /about/news/people-in-urban-areas-have-worse-hay-fever-symptoms-analysis-suggests/ /about/news/people-in-urban-areas-have-worse-hay-fever-symptoms-analysis-suggests/561356People living in urban areas report significantly worse hay fever symptoms according to the first study to compare pollution levels with the severity and duration of real-time symptoms.

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People living in urban areas report significantly worse hay fever symptoms according to the first study to compare pollution levels with the severity and duration of real-time symptoms.

Vlogٷ led team studied 36,145 symptom reports submitted over 5 years – from 2016 to 2020 - by over 700 Britons using a citizen science application called Britain Breathing.

The study, published in Scientific Reports today (insert date), compares self-reported allergy symptoms in urban and rural locations.

The severity of three symptoms captured by the ap: runny nose, sore eyes and wheezy breathing, were roughly twice as severe in urban areas than in rural ones across all years.

The study combined pollution measurements and pollen and meteorological data taken from the UK Met Office with the real-time, geo-positioned reports to examine the relationship between symptom severity and air quality.

The analysis shows that urban areas record significantly higher symptom severity and longer symptom duration for all years except 2017. Rural areas did not record significantly higher symptom severity in any year.

Symptom reports were labelled as urban or rural using land-use data from the UK’s Office for National Statistics.

Symptom severity was significantly correlated with ozone levels. Ozone has previously been linked to respiratory problems.

 

A potential reason for 2017 being an exception could be, argue the team, that the number of days with moderate or higher O3 levels dropped slightly that year before rising sharply and staying relatively high in subsequent years.

And 2017 was warmer and wetter in 2017 than the other years, which may have had an effect, either on pollen counts, pollution or participants’ biological reactions they add.

One of the study authors- immunologist Professor Sheena Cruickshank said: “The worldwide prevalence of allergic respiratory disease has risen considerably in recent years.

“However hay fever affects people differently and can change over a lifetime and data is lacking on how environmental factors may influence this.

“This study provides evidence that urban surroundings may exacerbate hay fever and asthma symptoms.

“It also provides a broader picture of chronic health issues experienced by hay fever and asthma sufferers, as opposed to only observing those with more acute and/or problematic reactions.

“These differences in allergy symptoms may be due to variation in the levels of pollutants, pollen counts and seasonality across land-use types.”

Professor of Computer Science Caroline Jay said: “The relationship between where people lived and the symptoms they experience was clear, but why people experience worse symptoms in urban areas is complex. There may be many aspects of the city environment that have a negative impact on respiratory health.”

#BritainBreathing a collaboration between the Royal Society of Biology, the British Society for Immunology, the Alan Turing Institute and Vlogٷ, aims to help the one in four people in the UK who suffer from seasonal allergies like hay fever and asthma. If you want to take part, download Britain Breathing on Google Play or the Appstore

The paper A comparison of experience sampled hay fever symptom severity across rural and urban areas of the UK is available

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Wed, 22 Feb 2023 15:07:00 +0000 https://content.presspage.com/uploads/1369/0bbbcb3b-2274-412f-ad6c-225d39a871c6/500_young-man-holding-tissue-paper-450w-144662081.jpg?10000 https://content.presspage.com/uploads/1369/0bbbcb3b-2274-412f-ad6c-225d39a871c6/young-man-holding-tissue-paper-450w-144662081.jpg?10000
Brain tricked into thinking it is fasting to cope better with inflammation /about/news/brain-tricked-into-thinking-it-is-fasting-to-cope-better-with-inflammation/ /about/news/brain-tricked-into-thinking-it-is-fasting-to-cope-better-with-inflammation/535349Mice who have been tricked into thinking they are fasting manage inflammation more easily, according to neurobiologists at Vlogٷ and collaborators from the University of Naples ‘Federico II’, in Italy.

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Mice who have been tricked into thinking they are fasting manage inflammation more easily, according to neurobiologists at Vlogٷ and collaborators from the University of Naples ‘Federico II’, in Italy.

The study of mice and published in Current Biology is also the first to show that the well-established protective effects of fasting are at least in part mediated by the brain, rather than a lack of nutrients as generally thought.

Funded by the Medical Research Council, the scientific team show that tricking the brain into thinking it is fasting is sufficient to induce effects of real fasting in otherwise well-fed mice.

Scientist have long known that periodic fasting can help promote a range of health benefits including reducing the severity of chronic inflammation, immune system regeneration, alleviating side effects of chemotherapy and even promote longevity.

But the researchers now show it is possible to induce some of the beneficial effects of fasting in mice, without them actually fasting.

The team developed a way to switch on a group of about 5,000 specialist brain cells called AgRP neurons  -a tiny figure compared to the 70 million or so nerve cells in the whole brain   which are responsible for generating the feeling of hunger.

Using specialist imaging techniques they were able to visualise the effect of a systemic inflammation in the mice who’s specialist brain cells had been engineered to glow fluorescently.

Loss of appetite and negative energy balance are common features of infection and inflammation in all animals, but are thought to have protective roles by reducing nutrient availability to host and pathogen metabolism.

However, the team discovered that the AgRP neurons detect reduced level of nutrients and respond by sending back to the body signals which have anti-inflammatory effects. Artificially turning on these specialist brain cells was also sufficient to generate anti-inflammatory effects.

Senior of author Dr Giuseppe D’ Agostino from Vlogٷ said: “Though it can be seen as paradoxical, the beneficial effects of fasting during sickness are well known”.

“We have now discovered that the brain plays an important role in this mechanism.”

Dr Gabriella Aviello from the University of Naples added: “There is obviously a long way to go, but the hope is that if we can exploit this mechanism, there could be a way to develop fasting memetic therapies which generate the beneficial effects of fasting, in those medical conditions where calorie restrictions is less desirable or counterproductive.”

The paper Hypothalamic AgRP neurons exert top-down control on systemic TNF-α release during endotoxemia is available

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Mon, 03 Oct 2022 17:00:00 +0100 https://content.presspage.com/uploads/1369/500_brain-3.jpg?10000 https://content.presspage.com/uploads/1369/brain-3.jpg?10000
Jeff Bezos is looking to defy death – this is what we know about the science of ageing /about/news/jeff-bezos-is-looking-to-defy-death--this-is-what-we-know-about-the-science-of-ageing/ /about/news/jeff-bezos-is-looking-to-defy-death--this-is-what-we-know-about-the-science-of-ageing/490653Jeff Bezos is on a mission to conquer ageing. He has just from GlaxoSmithKline to help lead Altos Labs, the ambitious new anti-ageing company with billions of investment. So what does science really say about this? Could we beat ageing?

Ageing isn’t just a change in how we feel or look, ageing happens at a cellular level. In a lab culture dish, adult skin cells divide roughly 50 times before stopping. But skin cells from a newborn baby can divide 80 or 90 times. And on the flip side, cells from someone elderly divide only around .

Ageing is also evident in our genes. Our genetic material is modified over time – chemicals can be attached that change which genes are switched on or off. These are called , and they build up as we age. Another kind of change takes place at the ends of our cell’s DNA. Repeating segments of DNA called telomeres act like the plastic tip of a shoelace, preventing the twisted coils of genetic material from fraying at the ends or knotting together. But these telomeres shorten each time a cell divides. We don’t know if short telomeres are merely a mark of ageing, like grey hair, or are part of the process by which cells age.

Cells, chromosomes and telomeres

 

To keep alive and keep dividing, immune cells stop their telomeres shortening when they multiply, . This is probably a contributing factor in their apparent immortality. Drugs that stop telomerase from working also show (although cancer cells can evolve resistance).

Bigger question

Given that ageing has such a profound effect on our cells and genes – the effects mentioned here being just some examples – a much bigger question emerges: why does this happen? Why do we age?

It was once thought that ageing happened for the continuing evolution of species. In other words, the evolution of a species requires a turnover of individuals. However, one problem with this idea is that most life on Earth doesn’t ever reach old age. Most animals are killed by predators, disease, the climate or starvation. So an inbuilt limit on an animal’s lifespan may not be important to evolution.

Another view is that ageing is simply a side-effect of the damage that builds up over time caused by metabolism or exposure to ultraviolet light from the Sun. We do know that genes are damaged as we age, but it is not proven that this drives ageing directly. Another possibility is that ageing might have evolved as a defence against cancer. Since cells accumulate genetic damage over time, they may have evolved a process to not persist in the body for too long, in case this damage eventually causes a cell to turn cancerous.

As we age, some of the body’s cells enter a state called senescence, in which a cell stays alive but stops dividing. Senescent cells accumulate in the body over a lifetime – especially in the skin, liver, lung and spleen – and have both beneficial and detrimental effects.

They are beneficial because they secrete chemicals that help repair damaged tissue, but over a long period of time, as senescent cells increase in number, they can disrupt the normal structure of organs and tissues. These cells could be an underlying cause of many of the problems we associate with ageing. Mice in which senescent cells were cleared were profoundly delayed in showing .

We can describe a lot of what happens during ageing at the level of what physically happens to our genes, cells and organs. But the fundamental question of why we age is still open. In all likelihood, there is more than one correct answer.

Of course, nobody knows whether Bezos’s company can succeed in helping extend the human lifespan. But what is clear is that by studying ageing, exciting new discoveries are bound to emerge. Never listen to anyone who says the big questions have already been answered. As I’ve recently detailed in a book about new technology and the human body, , I’m confident that dramatic breakthroughs will profoundly change the experience of being human in the coming century.The Conversation

, Professor of Immunology,

This article is republished from under a Creative Commons license. Read the .

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Fri, 21 Jan 2022 13:20:34 +0000 https://content.presspage.com/uploads/1369/500_stock-photo-active-old-age-people-and-lifestyle-concept-happy-senior-couple-riding-bicycles-at-summer-park-707244118.jpg?10000 https://content.presspage.com/uploads/1369/stock-photo-active-old-age-people-and-lifestyle-concept-happy-senior-couple-riding-bicycles-at-summer-park-707244118.jpg?10000
The journey to a pig-heart transplant began 60 years ago /about/news/the-journey-to-a-pig-heart-transplant-began-60-years-ago/ /about/news/the-journey-to-a-pig-heart-transplant-began-60-years-ago/489681The journey to a pig-heart transplant began 60 years ago

On Friday, January 7 2022, David Bennett became the world’s first person to successfully receive a . The eight-hour-long operation by surgeons at the University of Maryland Medical Center in Baltimore, USA, was no doubt arduous. But it was a short final step in a 60-year-long journey to genetically alter the pig’s heart so that it would not be immediately rejected – a journey that began with a plane crash in Oxford in the summer of 1940.

It was a hot Sunday afternoon when Peter Medawar, then 25, enjoying garden life in Oxford with his wife Jean and eldest daughter Caroline, was startled by the sight and noise of a bomber flying low towards them. The plane crashed violently in a garden 200m away. The pilot survived but suffered horrific burns. Medawar had trained as a zoologist, but his recent research had been to find out which antibiotics were best at treating burns. For the pilot who just crashed, doctors were at their wits’ end in deciding the right medication and asked Medawar to help.

The visceral shock of pacing the war wounds hospital spurred the young Medawar to think and work to a degree of intensity that he hadn’t known he was capable of. He saw airmen with much of their skin incinerated, lying in agony: while their lives could be prolonged by new medical advances – blood transfusions and antibiotics - there was no way of treating these horrific burns.

When doctors transplanted skin from one person to the next, it was destroyed soon after. At the time, doctors didn’t think there was any fundamental problem, only that the actual practicalities had to be perfected – the cutting and sewing. But Medawar thought something else was the problem. He obtained a grant from the War Wounds Committee and left home to surround himself with the problem, spending two months in a cheap hotel to work with Scottish surgeon Tom Gibson in the Burns Unit of the Glasgow Royal Infirmary. Together, they set out to observe exactly what happened during transplant rejection.

Their first patient was a 22-year-old woman, named in papers only as Mrs McK. She had been rushed to the Glasgow Royal Infirmary with deep burns down her right side from falling against her gas fire. To treat her, one area of her wound was covered with skin from her thigh and another area with skin taken from her brother’s thigh. A few days later, under a microscope, Mrs McK’s immune cells had invaded the skin grafts taken from her brother. Days later, the brother’s grafts degenerated. Her immune cells had caused the rejection.

Next, back in Oxford, Medawar chose to test this carefully using rabbits. Taking 25 rabbits, he grafted pieces of skin from each one onto every other one. If you’ve ever wondered what it might take to win a Nobel prize, Medawar’s starts here - with an important idea to be tested by 625 operations on 25 rabbits (25 x 25 individual skin grafts).

He showed that skin could not be grafted between different rabbits. Crucially, he also showed that in the second round of grafts, rejection happened more quickly the second time around, the hallmark of an immune reaction. The revolution starts here because Medawar and his team discovered that transplantation can work as long as an immune reaction is stopped. Medawar worked before genes and proteins could be easily manipulated, but this is relatively easy nowadays.

In the limelight again

Science of the immune system is in the limelight today because of the current pandemic. But as the science of immunity progresses, there are other big spin-offs, like new ways of switching off immune responses for avoiding transplant rejection.

In fact, as I’ve detailed in a book, , so many scientific and medical breakthroughs are happening, from new cancer therapies to manipulating the body’s genes or microbiome, I think we are at the cusp of a revolutionary time in virtually every aspect of human biology.

Medawar’s name endures not only his work on transplantation but also because of the brilliance of his writing. Richard Dawkins calls him the “wittiest scientist ever” and dedicated his 2021 collection of essays to him. The day before his first stroke in 1969, Medawar ended a lecture with a quotation from the 17th-century philosopher Thomas Hobbes proclaiming that life is like a race and the most important thing is to be in it, to be fully engaged, ambitious and go-getting, to improve the world. Eighteen years later, that same quotation was engraved on his : “There can be no contentment but in proceeding.”The Conversation

, Professor of Immunology,

This article is republished from under a Creative Commons license. Read the .

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Thu, 13 Jan 2022 13:46:01 +0000 https://content.presspage.com/uploads/1369/500_heart.jpg?10000 https://content.presspage.com/uploads/1369/heart.jpg?10000
Student swims her way to silver in the Paralympics /about/news/student-swims-her-way-to-silver-in-the-paralympics/ /about/news/student-swims-her-way-to-silver-in-the-paralympics/471841An immunology student at Vlogٷ has won a Silver in the women's SB5 100m breaststroke at the Paralympics in Tokyo

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An immunology student at Vlogٷ has won a Silver in the women's SB5 100m breaststroke at the Paralympics in Tokyo

Grace Harvey, also came 6th in the SM6 individual medley final earlier in the week, and will also be competing in more events over the next few days.

From Ware in Hertfordshire, the swimmer, who has cerebral palsy and began swimming when she was 4, has no function in her lower legs, swimming without a kick and co-ordination difficulties in her upper limbs.

Dr Thomas Nuhse, her academic advisor at the University said: “Grace’s enthusiasm for science and the hard work she has put in alongside her full-on training has been an inspiration.

“All of us here at Manchester are thrilled to watch her compete at the Paralympics and are cheering her on. Go Grace!”

After watching the 2004 and 2008 Paralympic Games, she decided she wanted to compete and joined a club at age nine.

The swimmer follows a gruelling training regime: 8 pool sessions – around 16 hours, 3 gym sessions and 2 indoor rowing sessions.

“I wish I had more time to go home and see my family and friends. Swimming doesn’t really leave me much free time – but it’s worth it,” she told the University’s last year.

“My belief in the hard work will come out on top. But I also want to do myself and my family proud,” added the University of Manchester sports scholar, a scheme which supports high performing athletes.

In her first year of study she was a full-time student and a full-time athlete though in the second year she went part-time and I found the balance to easier.

This year she completed her second half of the second year and in September will be returning full time to finish her third year.

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Tue, 31 Aug 2021 08:51:10 +0100 https://content.presspage.com/uploads/1369/500_graceharvey.jpg?10000 https://content.presspage.com/uploads/1369/graceharvey.jpg?10000
Saying Grace: Student swimmer makes splash at Paralympics /about/news/saying-grace-student-swimmer-makes-splash-at-paralympics/ /about/news/saying-grace-student-swimmer-makes-splash-at-paralympics/471190An immunology student at Vlogٷ is to go for Paralympic glory as world number one when she starts in the swimming competition on Thursday (26/08/21).

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An immunology student at Vlogٷ is to go for Paralympic glory as world number one when she starts in the swimming competition on Thursday (26/08/21).

Grace Harvey, will be racing in the 200m IM (SM6), 100m breaststroke (SB5), her main events, and the 400m free (S6), 100m back (S6) and 50m butterfly (S6). She is world number one in the 100m breastroke SB5.

From Ware in Hertfordshire, her first race- the 200M IM (SM6) will be at 9:43

The 200m IM take place on days 2 of the Games 26th August and the 100m breastroke on day 4, the 28th august. Other events fall over days 6,9 and 10.

Grace, who has cerebral palsy and began swimming when she was 4, has no function in her lower legs, swimming without a kick and co-ordination difficulties in her upper limbs.

She has broken 11 British records, including the European record in the S7 200m IM which she broke swimming for the University at the 2018 British Universities & Colleges Sport championhips.

She is also European bronze medallist in the S6 100m backstroke and British number 1 in the 100m backstroke.

Dr Thomas Nuhse, her academic advisor at the University said: “Grace’s enthusiasm for science and the hard work she has put in alongside her full-on training has been an inspiration.

“All of us here at Manchester are thrilled to watch her compete at the Paralympics and are cheering her on. Go Grace!”

She is currently training to become a Mental Health Champion for the British Para-Swimming team.

Last year she  revealed what it was like to walk for the first time in a robotic suit telling the BBC she was "overwhelmed" by the experience, adding: “had experienced the life that I was never destined for."

She was invited to Suzuka University to use their cyborg technology and was given the chance to try out a walking suit.

After watching the 2004 and 2008 Paralympic Games, she decided she wanted to compete and joined a club at age nine.

The swimmer follows a gruelling training regime: 8 pool sessions – around 16 hours, 3 gym sessions and 2 indoor rowing sessions.

“I wish I had more time to go home and see my family and friends. Swimming doesn’t really leave me much free time – but it’s worth it,” she told the University’s last year.

“My belief in the hard work will come out on top. But I also want to do myself and my family proud,” added the University of Manchester sports scholar, a scheme which supports high performing athletes.

In her first year of study she was a full-time student and a full-time athlete, though in the second year she went part-time, finding, she said, the balance easier to manage. This year she completed her second half of the second year and in September will be returning full time to finish her third year.

  • Dame Sarah Storey has won Great Britain’s first gold medal of  2021 at the . Storey  won the 3000 metre individual pursuit, after beating compatriot Crystal Lane-Wright. The win takes her total haul to 15 Paralympic golds – one short of swimmer Mike Kenny’s British record. She was awarded an honorary degree at the University in 2012. 
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Wed, 25 Aug 2021 13:08:00 +0100 https://content.presspage.com/uploads/1369/500_graceharvey.jpg?10000 https://content.presspage.com/uploads/1369/graceharvey.jpg?10000
Dedicated student Aimee takes Olympics in her stride /about/news/dedicatedstudent-aimee-takes-olympics-in-her-stride/ /about/news/dedicatedstudent-aimee-takes-olympics-in-her-stride/467045University of Manchester students and staff will be cheering along talented runner Aimee Pratt, who competes for team GB in the 3000m steeplechase on Sunday (August 1).

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University of Manchester students and staff will be cheering along talented runner Aimee Pratt, who competes for team GB in the 3000m steeplechase on Sunday (August 1).

The Anatomical Sciences student has gone from strength to strength, winning the 2020 British Championships in a time of 9 minutes 30.73 seconds, the eighth-fastest in the world last year.

Dr Bipasha Choudhury, Senior Lecturer in Anatomy and her personal advisor said: “Aimee is a hardworking and thoughtful student who puts 100% effort into her academic studies.

“The dedication she shows to her athletic training and her academic studies is a real testament to her determination to succeed in everything she tackles. We wish her every success in Tokyo.”

And Professor Tokiharu Takahashi, currently in Tokyo, has been teaching the athlete in his tutorial class since last October.

He said: “In the midst of the pandemic and with no prospect of holding the Games, while studying the complicated human anatomy, Aimee has tenaciously trained and finally made it this far.

“She is truly an Olympian and we, the anatomy tutorial group, wish her all the best. Go for it Aimee!”

Aimee, who runs for Sale Harriers, was at the 2020 Tokyo Olympic Games.

After running the consideration time for GB selection earlier, .

Aimee, from Stockport, has been running the steeplechase since 2014 thanks to the work of the Diane Modahl Sports Foundation.

The foundation created and run by Modahl - a former Commonwealth 800m champion - works with disadvantaged children from across the North West of England.

Aimee went along for fun, she told the website three point start, and after a few months was introduced to Diane’s husband, who is now her coach Vicente.

“One of the first things he said to me was that I had the potential to be a world class athlete, I was completely naive to whatever that meant but just enjoyed the challenge of training and competing,” she told the website.

Aimee ran for Vlogٷ, setting a British Universities and Colleges Sport championship record when she won gold in the 2019 BUCS 2000m Steeple Chase.

“You’ve been a massive support”, she told them in a tweet after the event.

She told Vinco in an interview last year: “2020 has been very strange and with the pandemic cancelling the European Championships and delaying the Olympic Games until 2021, I found it very hard early on in lockdown.

“I was just so excited to see the season opening up and that’s just got me back on track.”

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Fri, 30 Jul 2021 14:29:00 +0100 https://content.presspage.com/uploads/1369/500_aimeepratt.jpg?10000 https://content.presspage.com/uploads/1369/aimeepratt.jpg?10000
Books charts revolution of the science of human health /about/news/books-charts-revolution-of-the-science-of-human-health/ /about/news/books-charts-revolution-of-the-science-of-human-health/463322A leading scientist has charted the recent and dramatic breakthroughs in our understanding of the body in a new book out tomorrow (July 1).

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A leading scientist has charted the recent and dramatic breakthroughs in our understanding of the body in a new book out today (July 1).

In The Secret Body published by Vintage Books, Professor Dan Davis from Vlogٷ tells how new biology offers boundary-breaking possibilities for intervention in the human body, from our brains and genes to our microbiomes and immune systems.

Praised by Alice Roberts, Bill Bryson and Brian Cox, the book argues that this new revolution will profoundly change the experience of being human in the coming century.

Radical possibilities, immunologist Prof Davis tells us, have been made real thanks to decades of work by scientists.

Their breakthrough discoveries are transforming our understanding of how the body works, what it is capable of and how we might manipulate it, he says.

He describes, for example, how we are now able is to find out, years in advance, if we are likely to get certain cancers.

And how biology can now give us bespoke understanding of our genes, organs and cells and make drugs that can improve our cognition and acquire new skills.

He said: “‘Everything is kicking off in human biology. Radical new insights are emerging in our understanding of cells, embryos, the human brain, the microbiome, genes and so much more. It feels to me that human biology is just like how physics was in the early 1900s, when Einstein and others opened up quantum physics.

“Nowadays, our level of understanding of the human body is incomparable to what it was just a few years ago and we’ll be living with the consequences of that for decades to come. We can already understand and manipulate ourselves in ways that, only a few decades ago, no one could have dreamed.”

He added: “These boundary-breaking possibilities will confer unprecedented powers over health, childhood development, our cognitive and physical abilities, and affect every aspect of how we live our lives and think about ourselves.’’

“And we all will face previously unthinkable choices with consequences we have yet to understand.”

, discussion with Robin Ince takes place on book launch day July 1. Public lecture at , July 6

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Wed, 30 Jun 2021 10:23:00 +0100 https://content.presspage.com/uploads/1369/500_secretbodyrgbsubtitle.jpg?10000 https://content.presspage.com/uploads/1369/secretbodyrgbsubtitle.jpg?10000
Women’s stronger immune response could protect from some skin cancers /about/news/womens-stronger-immune-response-could-protect-from-some-skin-cancers/ /about/news/womens-stronger-immune-response-could-protect-from-some-skin-cancers/460170Women may have a stronger immune response to a common form of skin cancer than men, according to early research on mice and human cells.

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Women may have a stronger immune response to a common form of skin cancer than men, according to early research on mice and human cells.

Led by University of Manchester scientists at the Cancer Research UK Manchester Institute, the team publish their findings in Clinical Cancer Research.

The study is funded by The Wellcome Trust, Cancer Research UK and the Royal Society.

Men have more skin squamous cell carcinoma (cSCC) than females and their tumours are more aggressive. It is not clear if this is linked to more exposure to sunlight. This study used animals to explore this question.

The study found male mice developed more aggressive tumours than females, despite receiving identical treatments.

Immune cell infiltration and gene expression related to the anti-cancer immune system were increased in female mouse skin and tumours, suggesting a protective effect of the immune system.

In keeping with the animal study, 931 patient records collected from four hospitals in Manchester, London and France, the researchers identified that while women commonly have a more mild form of cSCC compared to men, immunocompromised women develop cSCC in a way more similar to men

That suggests the protective effect of their immune system may have been compromised.

The results in human patients were confirmed in a further cohort of sun-damaged skin from the USA. In this cohort, human epidermal cells confirmed women’s skin activated immune-cancer fighting pathways and immune cells at sites damaged by sunlight.

Furthermore, the USA cohort showed two types of human T Cells - CD4 and CD8- which are important in our immune response to skin cancer- were twice as abundant in women as in men.

The differences in male and female immunosuppressed mice and human skin cells were studied by a technique called RNA sequencing.

“It has long been assumed that men are at higher risk of getting non-melanoma skin cancer than women” said Dr Amaya Viros, from Vlogٷ.

“Other life-style and behavioural differences between men, such as the type of work or exposure to the sun are likely to be significant.

“However, we also identify for the first time the possible biological reasons, rooted in the immune system, which explains why men may have more severe disease.

“Although this is early research, we believe the immune response is sex-biased in the most common form of skin cancer, and highlights that female immunity may offer greater protection than male immunity.”

Dr Viros added: “We can’t yet explain why women have a more nuanced immune system than men.

“But perhaps it’s reasonable to speculate that women’s evolutionary ability to carry an unborn child of foreign genetic material may require their immunological system to be very finely tuned and have unique skills.

“Very little is known about how sex differences affect incidence and outcome in infectious diseases, autoimmune disorders and cancer. More work needs to be done.

“But we feel this study has opened a window into this area, and could one day have important implications on other types of immunologically based diseases.

“And it suggests if doctors are to offer personalised treatment of cancer, then biological sex should be one of the factors they take into account.”

Dr Samuel Godfrey, Research Information Manager at Cancer Research UK said: “Research like this chips away at the huge question of why people respond to cancer differently. Knowing more about what drives immune responses to cancer could give rise to new treatment options and show us a different perspective on preventing skin cancer.”

An embargoed copy of the paper Female immunity protects from cutaneous squamous cell carcinoma, published in Clinical Cancer Research, is available .

DOI: 10.1158/1078-0432.CCR-20-4261

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Thu, 03 Jun 2021 15:41:00 +0100 https://content.presspage.com/uploads/1369/500_skin.jpg?10000 https://content.presspage.com/uploads/1369/skin.jpg?10000
Altered immune signature linked to Long-Covid /about/news/altered-immune-signature-linked-to-long-covid/ /about/news/altered-immune-signature-linked-to-long-covid/447820University of Manchester scientists have discovered a persistent alteration in the immune system of patients, six months after they have been hospitalised for Covid-19 which could be associated with poorer health outcomes.

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University of Manchester scientists have discovered a persistent alteration in the immune system of patients, six months after they have been hospitalised for Covid-19, which could be associated with poorer health outcomes.

The study, published in the journal , examines the impact of a SARS-CoV-2 infection on the immune system of hospitalised patients in the period after a Covid-19 infection, once they have been discharged.

The team - based at the University’s Lydia Becker Institute of Immunology and Inflammation and supported by the UK Coronavirus Immunology Consortium (UK-CIC)- identified an immunological signature occurring in some of the patients that was associated with unresolved chest x-rays, indicating those patients had a poorer clinical outcome.

The researchers therefore identified immune characteristics in convalescent COVID-19 patients are associated with negative impacts on subsequent health.

The team compiled the immune cell characteristics of over 80 convalescent patients recruited from Manchester hospitals between July and October 2020.

They found that changes to B cells - a type of lymphocyte - that occur during the peak of COVID-19 hospitalisation were largely restored by 6 months of convalescence. However, changes to T cells, another lymphocyte, persisted into COVID-19 convalescence.

Study author Dr Joanne Konkel from Vlogٷ said: “Our study details persistent immune alterations in previously hospitalised COVID-19 patients up to 6 months after hospital discharge. Significantly, we outline an immune signature associated with poorer clinical outcomes in convalescent patients.

“Association, however, is not a causation, and what we now want to understand is what other long COVID symptoms this signature could be associated with and whether it could be used to identify the patients that should be most closely followed after hospital discharge.”

The signature present in the group of patients with the poorer clinical outcome was characterised by the team as having high levels of cytotoxic T cells – which can destroy other cells - as well as elevated production of special types of proteins called type-1 cytokines.

Study author Dr Madhvi Menon from Vlogٷ said: “It remains to be established if these immune alterations are unique to COVID-19, or whether they are also observed following other severe respiratory infections.”

The team hoped the results can be fed into larger UK wide studies, such as the University of Leicester led post-hospitalisation COVID-19 study known as PHOSP-COVID

PHOSP-COVID aims to better understand the interactions between immune cell changes and long COVID symptoms, as well as examine the clinical utility of the immune signature defined.

“Follow-up studies will determine whether this signature can provide a tool to identify acute COVID-19 patients at risk of Long COVID, enabling close monitoring and improved clinical management.”, said Dr Menon.

Study author Dr John Grainger from Vlogٷ and deputy Director of the Lydia Becker Institute said: “Given the vast numbers of previously infected individuals across the globe, it is vital to understand the impact of COVID-19 on the phenotype and functional potential of all immune cells.

“This will allow for better understanding of the long-term impacts of being hospitalised with COVID-19 on subsequent anti-pathogen or auto-inflammatory responses.”

The paper Alterations in T and B cell function persist in convalescent COVID-19 patients is published in

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Wed, 14 Apr 2021 15:04:00 +0100 https://content.presspage.com/uploads/1369/500_healthy-human-t-cell.jpg?10000 https://content.presspage.com/uploads/1369/healthy-human-t-cell.jpg?10000
COVID-19 immunity: how long does it last? /about/news/covid-19-immunity-how-long-does-it-last/ /about/news/covid-19-immunity-how-long-does-it-last/431845Millions of people across the world have been infected with SARS-CoV-2, the virus that causes COVID-19. Countries are also now embarking on to control the virus and protect their most vulnerable citizens. One of the biggest questions remaining is whether vaccination and/or prior infection with SARS-CoV-2 offers lasting protection against this deadly virus. The good news is that immunology is at last revealing some clues.

To understand whether immunity is possible – and why this has even been questioned – it is important to consider the nature of SARS-CoV-2. It is a betacoronavirus, and several betacoronaviruses already circulate widely in humans – they are most familiar to us as a cause of the common cold. However, immunity to cold-causing viruses is not long-lasting, leading many researchers to question whether longer term immunity to SARS-CoV-2 is possible.

However, studies considering the closely related betacoronaviruses that cause the diseases and offer a glimmer of hope. With these viruses, immunity has proved more durable. Could this be true for immunity to SARS-CoV-2 too?

Well-trained protection

The first of the body’s immune cells to respond to an infection are designed to attack the invading substances to try to control the infection’s spread and limit the damage done. The immune cells that respond later that are responsible for immunity are known as lymphocytes, which include . Lymphocytes need time to learn to identify the threat that they are facing, but once trained they can be rapidly deployed to seek and destroy the virus.

Our T cells and B cells work together to combat infection, but they have quite different functions that enable them to deal with a huge variety of threats. B cells make antibodies that neutralise infections. T cells are broadly divided into two types – T helper cells and cytotoxic T cells. Cytotoxic T cells directly kill viruses and cells that viruses have infected. T helper cells support the functioning of B cells and cytotoxic T cells. Collectively these are known as “effector” cells.

Virus cell in the body being attacked by tiny antibodies.

Studies have now demonstrated the that these effector cells play in the fight against COVID-19. Once the infection is gone, these cells should then die off in order to avoid causing excessive damage in the body.

But some effector cells persist. In an yet to be reviewed by other scientists, functional T cells have been detected six months after infection. Similarly, even patients who have had have detectable antibodies six to nine months . However, antibodies do wane over time, so these antibodies against SARS-CoV-2 could eventually disappear.

Remembering the danger

Such discoveries raise real optimism about protection from reinfection. But what happens if or when effector lymphocyte levels finally drop off? Well, our immune system has another trick up its sleeve to protect us for the long term, even after people’s effector cells and antibody levels have fallen. Once lymphocytes have been trained to deal with a virus, a pool of the cells remember it and are kept for the future. These “memory” cells can then be rapidly deployed if the threat is encountered again.

Memory cells are incredibly powerful tools for our immune system and can be very long-lived, with studies showing memory B cells for smallpox persisting at least 60 years after and for Spanish flu at least 90 years after the . In order to understand whether long-term immunity to SARS-CoV-2 is possible, it’s therefore critical to consider not just effector cells but all types of memory cells – B, T helper and cytotoxic T memory cells.

Fortunately, memory cells can be identified by specific structures and proteins that they express on their surfaces, enabling researchers to distinguish them from effector cells. Now that COVID-19 has been with us for a year, researchers are becoming able to make great leaps in understanding about memory responses to COVID-19. Evidence is emerging of lasting six to nine months after infection, and a recent preprint study (yet to be reviewed by other scientists) has also identified what appear to be .

Studies have also been investigating whether prior exposure to the virus confers protection, with showing that in the UK’s second wave, previously infected health workers were either completely protected from reinfection or were asymptomatic if they picked up the virus again. Such observational studies give real hope for the durability and potential of protective immunity.

We still have much to learn about the immunology of COVID-19, but the pace of research is astounding, and the more we learn, the more we are empowered to beat this virus. Our immune system is incredibly powerful, and these studies showing persistent immune responses nine months after infection are real cause for celebration. They give us confidence that, with vaccination, we have a real chance to win the war against COVID-19.The Conversation

, Professor in Biomedical Sciences,

This article is republished from under a Creative Commons license. Read the .

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Mon, 11 Jan 2021 15:09:32 +0000 https://content.presspage.com/uploads/1369/500_sars-cov-2-without-background.png?10000 https://content.presspage.com/uploads/1369/sars-cov-2-without-background.png?10000
‘Is it safe to have more than one type of COVID vaccine?’ and other questions answered by an immunologist /about/news/is-it-safe-to-have-more-than-one-type-of-covid-vaccine-and-other-questions-answered-by-an-immunologis/ /about/news/is-it-safe-to-have-more-than-one-type-of-covid-vaccine-and-other-questions-answered-by-an-immunologis/427525If we are ever to return to some semblance of normality, then the world’s population needs to be immune to SARS-CoV-2, the virus that causes COVID-19. But with so , questions are undoubtedly going to be raised, such as can I still have a vaccine if I have been involved in a trial testing other versions? And, what if I’ve already had COVID – do I still need a vaccine?

A basic understanding of immunology can answer all these questions. All COVID vaccines try to generate an immune response to proteins the virus needs to enter your cells. Whether this is by using a harmless virus carrying the protein that mimics SARS-CoV-2 but doesn’t replicate, or by using the genetic code for those proteins (a messenger RNA), the outcome is the same. The protein critical to stopping SARS-CoV-2 is displayed, recognised by the immune system, and the body produces antibodies and T cells that are then ready to stop future infection.

Is it OK to have a different second dose?

A booster vaccination enhances the quality of the immune response and sends a reminder about the virus. It doesn’t matter if the vaccine used to prime the immune system is different from the one used to boost, as long as they both contain the critical viral protein.

A person receiving a vaccine.

A booster shot is like a reminder to your immune system to be on the lookout for a particular bug.

Booster vaccinations are common, and the time interval between them varies. For example, a booster for tetanus is advised whereas vaccines for or measles are one-shot wonders – a booster is not needed.

Only by studying the immune response in people who have been vaccinated, will we be able to tell when and if further booster vaccinations are needed. This will be determined by measuring SARS-CoV-2 specific antibody and T cell responses in a sample of blood. It is possible that certain groups, such as older people, might need a different booster strategy – and this will take time to work out.

What if I’ve already had a trial vaccine?

If you’ve taken part in a COVID vaccine trial, it could give you a head start on the prime/boost approach, and you could reach the required immunity threshold quicker. Alternatively, your trial vaccination may have been so effective that the non-trial version of the vaccine isn’t necessary.

It is important for vaccine developers to follow up people who have had the vaccine to see how their immune system has reacted and whether or not the vaccine gave them immunity. This follow up should be conducted over a long period and encompass different sections of the population: young, old, different ethnic groups, and patients on drugs that dampen the immune system (such as chemotherapy).

What if I’ve had COVID?

Even if you have recovered from COVID-19, you can still benefit from vaccination. There in hospitalised patients that the infection was so overwhelming that the immune response became exhausted and so immune memory to the virus was not created efficiently. Also, if you had a very mild infection, your immune system may not have reached the point of laying down immune memory. So vaccination could be beneficial, regardless of whether you experienced severe or mild disease.

Though vaccination is a choice, don’t forget that vaccines have been around a long time and have . The risk of getting COVID and its awful and often long-term side-effects outweigh any theoretical risk of a vaccine.The Conversation

, Professor of Inflammatory Disease,

This article is republished from under a Creative Commons license. Read the .

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Mon, 07 Dec 2020 15:08:21 +0000 https://content.presspage.com/uploads/1369/500_file-20201204-13-vgjp4udnu.jpg?10000 https://content.presspage.com/uploads/1369/file-20201204-13-vgjp4udnu.jpg?10000
A new study suggests coronavirus antibodies fade over time – but how concerned should we be? /about/news/a-new-study-suggests-coronavirus-antibodies-fade-over-time--but-how-concerned-should-we-be/ /about/news/a-new-study-suggests-coronavirus-antibodies-fade-over-time--but-how-concerned-should-we-be/420883 suggests that levels of antibodies against the coronavirus have declined across the UK population since testing began. Having randomly sampled 365,000 people across the country, the React2 study – which is yet to be peer reviewed – estimates that 6% of the UK population had antibodies against the virus in late June, but that this had fallen to 4.4% by September.

If antibodies fade over time, how worried should we be? Does this mean we cannot be immune to COVID-19? To answer this question, we need first to consider what antibodies are and what they can tell us about immunity.

When we are infected, our immune system quickly responds to try and contain the threat and minimise the damage infection causes. This initial stage of immune reactivity is covered by immune cells known as innate cells that are resident in our tissues, which use a range of fairly generic strategies to both recognise and kill off the infection. But to truly deal with an infectious challenge, we need another part of our immune system – our lymphocytes.

Lymphocytes are more flexible cells that are “educated” to recognise and target a specific infectious agent. They come in – B lymphocytes, which make antibodies, and T lymphocytes, which can help the B cell response or directly kill the germs. Crucially, T and B lymphocytes work together to eradicate an infection.

Once a threat has been managed, a pool of these educated lymphocytes that know how to deal with that specific germ survive. These are known as memory cells. Memory cells are remarkably long-lived, patrolling our body ready for when they might again be needed. This whole system of lymphocyte responses is known as our adaptive immune response, and antibodies are only a portion of it.

So to properly understand and measure immunity after an infection, you would ideally assess both T and B lymphocytes and then see what happens when people face the same infection. But while testing for these cells is possible, it is expensive and impractical in large numbers of people, requiring costly reagents and detailed testing protocols.

As antibodies can be readily measured in blood samples, they are often used instead as an indication of whether there has been a good adaptive immune response. Over time, though, the levels of antibodies in our blood naturally fall – but this doesn’t necessarily mean protection is lost. Some of those educated memory cells should remain, including memory B cells that can quickly make more antibodies if needed. So the findings from React2 don’t necessarily mean that people are losing immunity to COVID-19.

For instance, have also looked at T cells and found in patients who have recovered from mild and severe COVID-19. We can therefore be somewhat optimistic that we could have some lasting protection against this disease.

We can also look at other viruses for clues. COVID-19 is caused by a beta coronavirus. There are several beta coronaviruses common in the human population – those that are most familiar cause the common cold. Long-lasting immunity to these cold-causing viruses , but immunity to more serious conditions caused by other beta coronaviruses – Mers and Sars – is . We do not yet know if immunity to the virus causing COVID-19 will be more akin to Sars or the cold-causing viruses, but the potential for longer lasting immunity to Sars and Mers offers some hope.

Finally, the React2 study looks at what happens after natural infections, but we should keep in mind that immunity generated by a vaccine might not be the same. Lymphocytes recognise germs by selecting some of their unique features to remember and react to and this matching process can be influenced by many factors, such as how the features are presented to lymphocytes or the available lymphocytes that recognise that feature. Although this allows for massive flexibility in the germs that can be recognised, it might not always result in the best viral killing in the future.

But with a vaccine, you can instead select the best bits of the pathogen to target in order to provoke the most effective T and B lymphocyte responses, which could in turn provoke bigger and better memory responses. This is being factored into the , with several vaccine candidates already being shown to promote .

Illustration of the SARS-CoV-2, showing the spike proteins on its surface Some vaccines are focusing the immune system on targeting the coronavirus’s spike proteins, shown here in orange.

However, if there is longer lasting immunity, it may not be present across all groups of people. Some, such as the elderly, are disproportionately affected by COVID-19, and the React2 study showed that older people had a . These results may be explained by the fact that many older people have – including the B lymphocytes needed for antibody protection.

Such findings emphasise the need to look at diverse groups of people to fully understand if immunity to COVID-19 is possible, particularly when developing vaccines. This is exactly what is being assessed in the happening now. Right now, we shouldn’t be overly worried. COVID-19 is a giant puzzle we are gradually unlocking. Every piece of the puzzle we master contributes to our growing knowledge and ability to beat this infection.The Conversation

, Professor in Biomedical Sciences,

This article is republished from under a Creative Commons license. Read the .

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Thu, 29 Oct 2020 08:14:15 +0000 https://content.presspage.com/uploads/1369/500_sars-cov-2-without-background.png?10000 https://content.presspage.com/uploads/1369/sars-cov-2-without-background.png?10000
Protein by which common skin bacteria trigger eczema identified /about/news/protein-by-which-common-skin-bacteria-trigger-eczema-identified/ /about/news/protein-by-which-common-skin-bacteria-trigger-eczema-identified/419111A decade-long study has identified the factor produced by a common species of skin bacteria that triggers eczema, in a breakthrough of our understanding of the condition.

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A decade-long study has identified the factor produced by a common species of skin bacteria that triggers eczema, in a breakthrough of our understanding of the condition.

The discovery of a missing link by an international team led by University of Manchester scientists could lead to new treatments for the sometimes debilitating skin condition which affects 20 to 30% of children.

Principle investigators Dr Peter Arkwright and Dr Joanne Pennock, both senior scientists at the University, identify ‘second immunoglobulin-binding protein’ - or ‘Sbi’ - as a unique trigger of eczema by Staphylococcus aureus - also known as golden Staph.

In a paper published in the prestigious Journal of Allergy and Clinical Immunology, they show that the bacterial species is unique in producing Sbi which triggers allergic inflammation in the skin.

The Leo Foundation-funded study for first time identifies Sbi as the molecule that induces rapid release of Interleukin-33, a key component of the immune response in childhood eczema.

“Our study shows beyond any doubt that Sbi is the dominant infective trigger of eczema and that is incredibly exciting,” said Dr Arkwright, who is also Consultant in Paediatric Allergy & Immunology at Royal Manchester Children’s Hospital, part of Manchester NHS Foundation Trust.

“Scientists have long known that Staphylococcus aureus is the dominant pathogen on human skin, causing the majority of skin and soft tissue infections worldwide.

“But only now do we understand that it is only because it expresses predominant virulence factor Sbi, that allergic eczema is triggered.

“There have been lots of dead ends and false leads, but after many years, we’ve finally found the missing link.

“We are extremely grateful to Professors Hiroshi Matsuda and Akane Tanaka for their collaboration, which contributed valuable results to this project.”

The search for the missing link involved mouse eczema model studies led by Tokyo University of Agriculture and Technology, and bench work on cells and human skin tissue at Manchester.

The scientists also studied six other species of staphylococci, as well as the common Group A strep which causes tonsillitis and scarlet fever, but none generated allergic responses.

In each part of the study, the results pointed to Sbi - first discovered in 1998 - as the trigger.

Dr Pennock, from Vlogٷ said: “Our primary aim was to understand why Staphylococcus aureus is so uniquely associated with allergic reactions in skin.

“The precise mechanism that drives the allergic pathology in eczema patients has been a mystery, until now.

Staphylococcus aureus expresses many virulence factors so finding the right protein was a challenge. We have shown that only golden Staph that expresses Sbi is capable of causing the allergic skin response.

”Now our aim is to learn more about Sbi in order to lay the groundwork for future non-steroid treatments. We are very grateful to the Leo Foundation for continuing to fund this exciting work. ‘’

The paper Staphylococcus aureus Second Immunoglobulin-Binding Protein drives atopic 2 dermatitis via IL-33 is published in the Journal of Allergy and Clinical Immunology

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Mon, 19 Oct 2020 17:00:00 +0100 https://content.presspage.com/uploads/1369/500_skin-1392555.jpg?10000 https://content.presspage.com/uploads/1369/skin-1392555.jpg?10000
Coronavirus reinfection cases: what we know so far – and the vital missing clues /about/news/coronavirus-reinfection-cases-what-we-know-so-far--and-the-vital-missing-clues/ /about/news/coronavirus-reinfection-cases-what-we-know-so-far--and-the-vital-missing-clues/419008As President Trump claims that he is and isolated reports emerge of reinfection, what is the truth about immunity to COVID-19?

To date, there have been of COVID-19 reinfection, with various other unverified accounts from around the world. Although this is a comparably small fraction of known to have been infected, should we be concerned? To unpick this puzzle, we must first consider what we mean by immunity.

How immunity works

When we are infected with any pathogen, our immune system quickly responds to try to contain the threat and minimise any damage. Our first line of defence is from immune cells, known as innate cells. These cells are not usually enough to eliminate a threat, which is where having a more flexible “adaptive” immune response comes into play – our lymphocytes.

Lymphocytes come in two main varieties: B lymphocytes, which make antibodies, and T lymphocytes, which include cells that directly kill the germy invaders.

As antibodies are readily measured in blood, they are often used to indicate a good adaptive immune response. However, over time, antibodies levels in our blood wane, but this doesn’t necessarily mean protection is lost. We retain some lymphocytes that know how to deal with the threat – our memory cells. Memory cells are remarkably long-lived, patrolling our body, ready to spring into action when needed.

Vaccines work by creating memory cells without the risk of a potentially fatal infection. In an ideal world, it would be relatively easy to create immunity, but it’s not always that straightforward.

Although our immune system has evolved to deal with a huge variety of pathogens, these germs have also evolved to hide from the immune system. This arms race means that some pathogens such as malaria or HIV are very tricky to deal with.

Infections that have spilled over from animals -– zoonotic diseases –- are also challenging for our immune system because they can be completely novel. The virus that causes COVID-19 is such a zoonotic disease, originating in .

COVID-19 is caused by a betacoronavirus. Several betacoronaviruses are already common in the human population – most familiar as a cause of the common cold. Immunity to these cold-causing viruses isn’t that but immunity to the more serious conditions, Mers and , is more durable.

Data to date on COVID-19 shows that antibodies can be detected three months after infection, although, as with Sars and Mers, antibodies gradually decrease .

Of course, antibody levels are not the only indication of immunity and don’t tell us about T lymphocytes or our memory cells. The virus causing COVID-19 is structurally similar to , so perhaps we can be more optimistic about a more durable protective response – time will tell. So how worried then should we be about reports of reinfection with COVID-19?

How worried should we be?

The handful of case reports on reinfection with COVID-19 don’t necessarily mean that immunity is not occurring. Issues with testing could account for some reports because “virus” can be detected after infection and . The tests look for viral RNA (the virus’s genetic material), and viral RNA that cannot cause infection can be shed from the body even after the person has recovered.

Conversely, false-negative results happen when the sample used in testing contains insufficient viral material to be detected – for example, because the virus is at a very low level in the body. Such apparent negative results may account for cases in which the interval between the first and second infection is short. It is hugely important, therefore, to use additional measures, such as viral sequencing and immune indicators.

Reinfection, even in immunity, can happen, but usually this would be mild or asymptomatic because the immune response protects against the worst effects. Consistent with this is that most verified cases of reinfection reported either no or mild symptoms. However, one of the latest verified cases of reinfection – which happened just 48 days after the initial infection – actually had a more severe response to .

What might account for the worse symptoms the second time round? One possibility is the patient did not mount a robust adaptive immune response first time round and that their initial infection was largely contained by the innate immune response (the first line of defence). One way to monitor this would be to assess the antibody response as the type of antibody detected can tell us something about the timing of infection. But unfortunately, antibody results were not analysed in the recent patient’s first infection.

Another explanation is that different viral strains caused the infections with a subsequent impact on immunity. Genetic sequencing did show differences in viral strains, but it isn’t known if this equated to altered immune recognition. Many viruses share structural features, enabling immune responses to one virus to protect against a similar virus. This has been suggested to account for the lack of symptoms in young children who frequently get colds caused by betacoronaviruses.

However, a , yet to be peer-reviewed, found that protection against cold-causing coronaviruses did not protect against COVID-19. In fact, antibodies recognising similar viruses can be dangerous – accounting for the rare phenomenon of antibody-dependent enhancement of disease (ADE). ADE occurs when antibodies enhance viral infection of cells with potentially life-threatening consequences.

It should be emphasised, though, that antibodies are only one indicator of immunity and we have no data on either T lymphocytes or memory cells in these cases. What these cases emphasise is a need to standardised approaches in order to capture the critical information for robust evaluation of the threat of reinfection.

We are still learning about the immune response to COVID-19, and every piece of new data is helping us unpick the puzzle of this challenging virus. Our immune system is a powerful ally in the fight against infection, and only by unlocking it can we ultimately hope to defeat COVID-19.The Conversation

, Professor in Biomedical Sciences,

This article is republished from under a Creative Commons license. Read the .

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Fri, 16 Oct 2020 13:34:33 +0100 https://content.presspage.com/uploads/1369/500_sars-cov-2-without-background.png?10000 https://content.presspage.com/uploads/1369/sars-cov-2-without-background.png?10000
Cure found for rare form of inflammatory bowel disease /about/news/cure-found-for-rare-form-of-inflammatory-bowel-disease/ /about/news/cure-found-for-rare-form-of-inflammatory-bowel-disease/418505A rare genetic condition which causes inflammatory bowel disease can be successfully treated by bone marrow transplant, according to University of Manchester and researchers.

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A rare genetic condition which causes inflammatory bowel disease can be successfully treated by bone marrow transplant, according to University of Manchester and researchers.

The disease, called G6PC3 deficiency, affects around one in a million people and causes inflammation of the bowel, as well as lung infections.

The team also showed that in affected patients, white blood cells called neutrophils trigger inflammation when exposed to gut bacteria, despite treatment with commonly available biological therapies.

The patients were treated at the Royal Manchester Children’s Hospital – part of Manchester University NHS Foundation Trust (MFT) – one of the world’s leading centres for paediatric bone marrow transplantation, under the direction of Professor Rob Wynn.

The study is published in .

Dr Anu Goenka carried out the laboratory work as part of his PhD. He was funded by both a Medical Research Council Clinical Research Training Fellowship, as well as a Fellowship from the European Society for Pediatric Infectious Diseases (ESPID).

G6PC3 is important in sugar metabolism, critical for providing energy for neutrophils, which struggle to divide and function when it is deficient.

Neutrophils – which form pus - are deployed by the body to remove bacteria, particularly in the gut and lungs.

The team examined neutrophil function and response to bone marrow transplant in four children with G6PC3 deficiency-associated IBD.The children’s IBD had failed to respond to other immune therapies including steroids and biologics.

After the treatment, the symptoms of IBD went into remission in all of the patients. Three of the patients are now three to four years post-transplant and still in remission.

Dr Peter Arkwright, Senior Lecturer at Vlogٷ and Consultant in Paediatric Immunology Royal Manchester Children’s Hospital, led the study.

Most patients stay in isolation in a ward for three to four weeks before going home to isolate for a further few months.

Professor Tracy Hussell, Director of the Lydia Becker Institute of Immunology and Inflammation and researcher, was co-lead.

Dr Arkwright said: “Although IBD caused by G6PC3 deficiency is extremely rare and difficult to diagnose, it’s thrilling that we have found a way to successfully treat it in these four children.

“It’s rare to say a cure has been found for any disease, but I think in this case, it’s perfectly accurate to say this.

“Our paper has also shown beyond any doubt that IBD G6PC3 deficiency can cause IBD.”

Children with the deficiency are often diagnosed in the first few years of their life, though some aren’t diagnosed until they are 11 and 12.

And because of difficulties in detecting the disease or receiving transplant, adults may also be affected.

Bone Marrow transplant donors are either relatives or members of a bone marrow registry.

The donated marrow is infused into a vein once the child has had chemotherapy.

Around 10 days after transfusion, new neutrophils appear – although the immune system takes between three and four months to recover.

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Tue, 13 Oct 2020 15:13:00 +0100 https://content.presspage.com/uploads/1369/500_doctor.jpg?10000 https://content.presspage.com/uploads/1369/doctor.jpg?10000
Role of bone marrow immune cells in COVID-19 revealed /about/news/role-of-bone-marrow-immune-cells-in-covid-19-revealed/ /about/news/role-of-bone-marrow-immune-cells-in-covid-19-revealed/415747White blood cells called monocytes released into the blood from bone marrow have abnormal features in people who have COVID-19, according to a new study by University of Manchester immunologists at the .

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White blood cells called monocytes released into the blood from bone marrow have abnormal features in people who have COVID-19, according to a new study by University of Manchester immunologists at the .

And the team from the (CIRCO) consortium say the abnormalities are greater in patients with severe infection.

By spotting the abnormal monocytes early, doctors may be able to predict which patients are more likely to develop severe disease.

The study provides the strongest evidence yet that monocytes may be an important therapeutic target for a COVID-19 treatment.

It is not yet clear, say the team, if abnormal monocytes are released from the bone marrow or if the changes happen after they enter the blood.

However, treatments preventing their release from bone marrow may help reduce the exaggerated immune response that contributes to poor outcomes in patients with severe COVID-19.

The paper in Science Immunology is the first to be published by the consortium, based at Vlogٷ.

Scientists already know that monocytes - the largest type of white blood cell - are an important component in the lung during infection and play roles in protection and repair.

The team analysed over a hundred blood samples from COVID-19 patients admitted to four hospitals across Greater Manchester to search for biomarkers that signal progression to severe disease at various points in their hospital stay.

Dr John Grainger, Deputy Director of the Lydia Becker and a senior author on the study said: “Our work once again highlights the importance of the innate immune system in COVID-19, we’re excited to be able to finally share the results of our study and hope that it can better inform treatments for this devastating disease”.

The CIRCO consortium draws together immunological expertise from the Lydia Becker Institute with clinicians and research nurses at Salford Royal, Wythenshawe, North Manchester and Manchester Royal NHS Trusts.

It was set-up during the first wave of the pandemic to collect longitudinal samples from patients with diagnosed COVID-19; studying their immune response from hospital admission through to outcome.

The study was in part supported by a rapid response COVID-19 award from

Prof. Tracy Hussell, Director of the Lydia Becker Institute, added: “Thanks to all members of the CIRCO team for their hard work on this study it has been a great example of scientists and clinicians working together to give new insight into this infection”.

The paper Longitudinal immune profiling reveals key myeloid signatures associated with COVID-19 is available 

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Wed, 23 Sep 2020 11:55:00 +0100 https://content.presspage.com/uploads/1369/500_monocyte.png?10000 https://content.presspage.com/uploads/1369/monocyte.png?10000
UK Coronavirus Immunology Consortium to address key unanswered questions about immunity and COVID-19 /about/news/uk-coronavirus-immunology-consortium-to-address-key-unanswered-questions-about-immunity-and-covid-19/ /about/news/uk-coronavirus-immunology-consortium-to-address-key-unanswered-questions-about-immunity-and-covid-19/412340Immunologist Professor Tracy Hussell from Vlogٷ and a team from across the UK will be investigating the nature of COVID-19 infection outside hospital.

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Today (Friday 28 August) sees the launch of the new UK Coronavirus Immunology Consortium (UK-CIC), which aims to answer key questions on how the immune system interacts with SARS-CoV-2 to help us fight COVID-19 and develop better diagnostics, treatments and vaccines.

Identifying how the immune system responds to SARS-CoV-2 is critical to understanding so many of the unknowns around this novel virus – for example, why does it make some people sick and not others, what constitutes effective immunity and how long might that immunity last? The immune system is extremely complex and to make rapid and effective progress in our knowledge, a cohesive, nationally co-ordinated approach is required.

To address this need, the UK Coronavirus Immunology Consortium has received £6.5million of funding over 12 months from UK Research and Innovation (UKRI) and the National Institute for Health Research (NIHR), the largest immunology grant awarded to tackle the COVID-19 pandemic. UK-CIC aims to deliver meaningful benefit for public health by providing insights critical for improving patient management, developing new therapies, assessing immunity within the population and developing diagnostics and vaccines.

Professor Tracy Hussell, Theme Lead for UK-CIC, from Vlogٷ said: “The immune system is one of the most complicated systems in the human body but understanding how it reacts during and after infection with SARS-CoV-2 is critical to our ability to control this pandemic.

“This immune system response not only dictates how quickly you can clear the virus but also how sick you will get, as well as how long any immunity generated to the virus might last. The UK Coronavirus Immunology Consortium wants to look at what happens on a cellular and molecular level when someone contracts COVID-19 and find out what exactly their immune system is doing. We will work with colleagues around the country to build our understanding of how different people react to COVID-19 with the ultimate aim of improving patient care at all levels.”

The UK-CIC aims to answer five key questions that will help the global coronavirus response.

  1. Why do people experience different symptoms to COVID-19 and what role does the immune system play in this?
  2. What constitutes immunity to COVID-19 and how long does it last?
  3. How does the immune system respond to SARS-CoV-2 on a molecular and cellular level and what happens when the immune system overreacts?
  4. Can infection with other mild coronaviruses (which cause the common cold) protect you from catching COVID-19 or will it make you more ill?
  5. How does SARS-CoV-2 hide from the immune system?

Prof Hussell and a team from across the UK will be investigating the nature of COVID-19 infection outside hospital. They will be asking why many people have been infected but show no symptoms, while others have manageable symptoms which do not need hospitalisation.

A second strand of the work will consolidate and generate genetic data from people who have had the disease, with the help of Prof Magnus Rattray Professor Computational and Systems Biology from Vlogٷ. The work will allow the researchers to identify biological risk according to gender, ethnicity and deprivation and other factors. And a final strand of the work will be to test the immune system and how it responds to the virus.

Prof Hussell added: “The UK Coronavirus Immunology Consortium is an unprecedented opportunity to understand this disease and build effective ways of treating it. We hope the public will come forward so we may examine their biology and learn from what has happened to them. Details of how to day that will be publishing in the coming weeks.

“We will be particularly interested in people who have tested positive but have had no symptoms, though we would also be happy to work with members of the public who have not been diagnosed with Covuid-19.

“Different institutions and the public are coming together to take this research forwards and we are excited at the prospect of making great strides in the fight against this disease.”

UK-CIC is jointly funded by UKRI and NIHR as part of their rolling call for research proposals on COVID-19. It is supported by the British Society for Immunology. The aims of UK-CIC were developed from the set out in May 2020 by the Academy of Medical Sciences and British Society for Immunology expert taskforce on immunology and COVID-19.

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Fri, 28 Aug 2020 00:04:00 +0100 https://content.presspage.com/uploads/1369/500_1920-stock-photo-female-medical-or-research-scientist-or-doctor-using-looking-at-a-test-tube-of-clear-solution-in-a-595303463.jpg?87513 https://content.presspage.com/uploads/1369/1920-stock-photo-female-medical-or-research-scientist-or-doctor-using-looking-at-a-test-tube-of-clear-solution-in-a-595303463.jpg?87513
Inflammation: the key factor that explains vulnerability to severe COVID /about/news/inflammation-the-key-factor-that-explains-vulnerability-to-severe-covid/ /about/news/inflammation-the-key-factor-that-explains-vulnerability-to-severe-covid/411730  

The severity of COVID-19 can vary hugely. In some it causes no symptoms at all and in others it’s life threatening, with to its very severe impacts.

The virus disproportionately and people who and who have conditions such as and . In the UK and other western countries, have also been disproportionately affected.

While many factors contribute to how severely people are affected, including , and environmental risks such as , it’s becoming clear that for some of these at-risk groups, it’s the response of their immune system – inflammation – that explains why they get so sick.

Specifically, we’re seeing that the risks associated with diabetes, obesity, age and sex are all related to the immune system functioning irregularly when confronted by the virus.

Inflammation can go too far

A common feature for many patients that get severe COVID is serious lung damage caused by an overly vigorous immune response. This is characterised by the creation of lots of inflammatory products called cytokines – the so-called cytokine storm.

Cytokines can be really powerful tools in the immune response: they can stop viruses reproducing, for example. However, some cytokine actions – such as helping bring in other immune cells to fight an infection or enhancing the ability of these recruited cells to get across blood vessels – can cause real damage if they are not controlled. This is exactly what happens in a cytokine storm.

Many white blood cells create cytokines, but specialised cells called monocytes and macrophages seem to be some of the biggest culprits in generating cytokine storms. When properly controlled, these cells are a force for good that can detect and destroy threats, clear and repair damaged tissue, and bring in other immune cells to help.

However, in severe COVID the way monocytes and macrophages work misfires. And this is particularly true in patients with diabetes and obesity.

Glucose fuels damage

Diabetes, if not controlled well, can result in high levels of glucose in the body. A showed that, in COVID, macrophages and monocytes respond to high levels of glucose with worrying consequences.

The virus that causes COVID, SARS-CoV-2, needs a target to latch onto in order to invade our cells. Its choice is a protein on the cell surface . Glucose increases the levels of ACE2 present on macrophages and monocytes, helping the virus infect the very cells that should be helping to kill it.

An immune cell releasing thousands of small cytokines. Cytokines, small proteins released by a number of immune cells, play a key role in directing the immune response. ,

Once the virus is safely inside these cells, it causes them to start making lots of inflammatory cytokines – effectively kick-starting the cytokine storm. And the higher the levels of glucose, the more successful the virus is at replicating inside the cells – essentially the glucose fuels the virus.

But the virus isn’t done yet. It also causes the virally infected immune cells to make products that are very damaging to the lung, such as reactive oxygen species. And on top of this, the virus reduces the ability of other immune cells – lymphocytes – to kill it.

Obesity also causes high levels of glucose in the body and, similar to diabetes, . Research has shown that macrophages from obese individuals are an for SARS-CoV-2 to thrive.

Other risks tied to inflammation

The same sort of inflammatory profile that diabetes and obesity cause is also seen in some older people (those over 60 years). This is due to a phenomenon known as .

Inflammageing is characterised by having high levels of pro-inflammatory cytokines. It’s influenced by a number of factors, including genetics, the microbiome (the bacteria, viruses and other microbes that live inside and on you) and obesity.

Many older people also have – the very cells that can specifically target and destroy viruses.

This all means that for some older people, their immune system is not only poorly equipped to fight off an infection, but it is also more likely to lead to a damaging immune response. Having fewer lymphocytes also means vaccines may not work as well, which is crucial to consider when planning a future COVID vaccine campaign.

Another puzzle that has been worrying researchers is why men seem so much more vulnerable to COVID. One reason is that cells in men seem to be more readily infected by SARS-CoV-2 than women. The ACE2 receptor that the virus uses to latch onto and infect cells is in men than women. Men also have higher levels of an enzyme called TMPRSS2 that promotes the ability of the virus to enter the cells.

Immunology is also offering some clues on the sex difference. It’s long been known that men and women differ in their , and this is true in COVID.

A (research that has not yet been reviewed) has tracked and compared the immune response to SARS-CoV-2 in men and women over time. It found that men were more likely to develop atypical monocytes that were profoundly pro-inflammatory and capable of making cytokines typical of a cytokine storm. Women also tended to have a more robust , which is needed for effective virus killing. However, increased age and having a higher body mass index reversed the protective immune effect in women.

Studies like these highlight how different people are. The more we understand about these differences and vulnerabilities, the more we can consider how best to treat each patient. Data like these also highlight the need to consider variation in immune function and include people of varied demographics in drug and vaccine trials.The Conversation

, Professor in Biomedical Sciences,

This article is republished from under a Creative Commons license. Read the .

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Fri, 21 Aug 2020 14:48:34 +0100 https://content.presspage.com/uploads/1369/500_don039tuseinflammationconversation.jpg?10000 https://content.presspage.com/uploads/1369/don039tuseinflammationconversation.jpg?10000
Coronavirus: how T cells are involved and what it might mean for vaccine development /about/news/coronavirus-how-t-cells-are-involved-and-what-it-might-mean-for-vaccine-development/ /about/news/coronavirus-how-t-cells-are-involved-and-what-it-might-mean-for-vaccine-development/393344Developing a vaccine is difficult at the best of times, but rarely have we been in a situation where basic knowledge about a virus has to be acquired so directly alongside the race to eradicate it. To understand how difficult this task is, we must appreciate the complexity of how our immune system responds to an infection.

The part of the immune response that can target germs precisely and provide long-term protection is called the adaptive immune response. Two types of white blood cell are important in this: T cells and B cells. These cells work together to orchestrate a targeted immune response. But the way they recognise and deal with germs is different.

Both T cells and B cells have an important receptor molecule on their surface, not so imaginatively called the T cell receptor and the B cell receptor. B cell receptors lock onto unique structural components of a germ, or an infected cell, directly. T cells, on the other hand, need other immune cells to chew up and present parts of the germ in small fragments, which can then be scrutinised.

So for any given germ, T cells and B cells see it differently. They also respond in different ways. Even T cells don’t just do one thing. Some – the cytotoxic T cells – attack infected cells directly, while others – the T helper cells – support immune responses by helping B cells produce antibodies.

All this complexity serves to attack different germs in different ways and helps prevent unintended damage to our body’s healthy cells and tissues, as it provides multi-step checks before an immune response is fully activated.

Getting T cells and B cells to respond to a germ takes time – usually several days following the initial infection. Once T and B cells have been sent to deal with a germ, the immune response subsides and long-lived memory versions of T cells and B cells are retained so that the appropriate response can be mounted much faster if the same germ is encountered again.

Vaccines try to mimic this natural process by provoking the development of long-lived memory T cells and B cells, without triggering the symptoms of a real infection. It’s not the case, though, that each type of vaccine stimulates a similar immune response. There are many types of vaccine and each will trigger a cascade of events that stimulate the immune system in a particular way.

Most vaccines will target B cells and the types of T cells that support antibody production. Yet for some infections, the antibody response may not be enough. In such cases, vaccines can also be developed to promote cytotoxic T cell activity, or perhaps a combination of both antibody and cytotoxic T cell immune responses.

Understanding the type of immune response that works best against a particular infection is important for vaccine design. And we are still learning about our adaptive immune response to the novel coronavirus.

Looking beyond spike proteins

The virus can be pictured as a small spiky ball that encapsulates genetic material. Many vaccines currently being tested aim to create an immune reaction against the protein molecules that make up the outer spikes. The spikes are critical for how the virus gets into human cells, so antibodies that lock onto those structures might stop the virus from entering cells. But the evidence is mounting that targeting other parts of the virus might also be useful.

A coronavirus with its telltale spike proteins jutting out from the surface.

A recent study – which has – assessed T cell memory responses in patients who had recovered from . Patients who had severe symptoms showed a stronger and more varied T cell response. Their T cells reacted to the virus’s spikes, but also to internal components of the virus – which have cumbersome names such as “receptor binding domains” and “nucleoproteins”.

In detail, cytotoxic T cells that could attack virus-infected cells directly seemed to target internal parts of the virus, whereas T helper cells, which support antibody production, reacted to viral surface molecules.

Having an immune response capable of detecting different aspects of a virus might make it harder for the virus to escape being detected. This is important to factor into the design of vaccines: maybe we will need cytotoxic T cells and B cells to target different parts of the virus. Indeed, a study in macaques showed that a vaccine candidate targeting only the viral spike protein induced good, but not complete, .

Vaccines that do not induce full immunity are still important, of course, because they can lessen the severity or duration of infection. This is why designing vaccines is a complex process that requires a good understanding of immune responses.

We are still learning about COVID-19 and questions remain as to whether complete protection against it is even possible.

Issues still to be tackled

Another area of debate is whether some protection can arise from being infected with another coronavirus. There is some similarity between the version of coronavirus causing the current pandemic and others that cause a mild cold.

Some studies show a , but others show . Differences in these results may be down to how immune responses were analysed, or variations between people who could have had different prior exposures. Either way, such conflicting observations highlight the complexities involved.

Concerns have also been raised about the possibility of vaccines eliciting a response that could, at least in principle, produce antibodies that help the virus get into cells – a phenomenon known as .

The pressure to develop a vaccine is huge. The rush must not override the need for safety. There are other issues we must also tackle – not least, the manufacturing and fair distribution of anything that works. But right now, understanding the human immune response to this virus is our best hope and our greatest challenge.The Conversation

, Professor in Biomedical Sciences, and , Professor of Immunology,

This article is republished from under a Creative Commons license. Read the .

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Thu, 11 Jun 2020 13:35:48 +0100 https://content.presspage.com/uploads/1369/500_conversationdonotuse.jpg?10000 https://content.presspage.com/uploads/1369/conversationdonotuse.jpg?10000
Coronavirus: we must step up research to harness immense power of the immune system /about/news/coronavirus-we-must-step-up-research-to-harness-immense-power-of-the-immune-system/ /about/news/coronavirus-we-must-step-up-research-to-harness-immense-power-of-the-immune-system/389887Many countries are moving to exit a lockdown triggered by COVID-19, but the virus has not gone away and there are real concerns that a second wave of infection could happen. We urgently need to understand more about how the body deals with this infection and what we can do to tackle it. Immunology has taken centre stage here in revealing what happens when our body fights this virus, and brings us the possibility of treatments and vaccines.

One of the most amazing things about our immune system is that it can fight germs it has never encountered before. We understand much about how this works, and this detailed knowledge seeds ideas about how COVID-19 could be tackled with a vaccine or other types of drugs, such as those that have made AIDS a disease that can be controlled. But we must be under no illusion – it will take time. There are seven known types of coronavirus that infect humans and we don’t have a vaccine against any of them.

Scientific understanding of COVID-19 is moving fast. We already know that the virus enters the body’s cells through a protein on cells called ACE2. ACE2 is highly prevalent in cells that line the airway.

Once inside the cells, the virus can exploit their machinery to create a viral production factory. A chain reaction builds up where new virus particles are released, which either infect more cells or can be expelled from the body to infect others.

The virus mainly moves from one person to another in respiratory droplets, sent out as we cough, sneeze or talk. This can happen before a patient has symptoms, which is one reason this particular virus has spread so effectively throughout the world. ACE2 is also present in gut cells and there are reports of viral shedding occurring in samples, suggesting a need for good personal hygiene, although for the moment this is only a potential route of transmission.

The virus spreads to others through respiratory droplets.

The process of infection causes signals which alert the immune system that there is a threat to deal with. Immune cells that live in the lung airways, such as macrophages, natural-killer cells and others, deal with the infection early on. Macrophages can also help repair the damage the infection causes and recruit other immune cells to the airways too. How macrophages are and how they may be important in what happens to each of us overall. The most severe cases of COVID-19 have been associated with macrophages that produce high levels of inflammatory protein molecules called cytokines, such as interleukin-6.

This early immune response probably can’t wholly eliminate the infection; we need other white blood cells to get involved. An enormous reservoir of immune cells is available, but only a few of these will be a good match to tackling this specific virus. Once the best match is established, these specific immune cells multiply. B cells make large quantities of antibody which can neutralise the virus directly and mark infected cells for attack. T cells also destroy the infected cells directly. This process of generating large numbers of the right immune cells happens in the lymph nodes, sometimes felt as “glands” which get swollen when this is happening.

There are many questions about whether or not people who have had the infection are immune afterwards and how we can detect this. Tests for our exposure to the virus rely on detecting this specific activity of our immune response, in the presence of antibodies. These antibodies can reveal if someone has been infected in the past but we do not yet know if this indicates that they have full or partial protection against future infections and so an “antibody passport” may not be useful.

Also, reports suggest that around 10%-20% of patients who have been infected have little or no detectable antibody in their blood and there are concerns about the reliability and validity of the antibody tests currently available. We urgently need to understand the role of antibodies, as well as other components of the immune response, and whether these can provide, or correlate with, protection against this infection.

It is not yet clearly understood why disease severity varies between people. Age is an important factor, which may partly be because the immune system changes as we age. Older people are more likely to have a background low level of inflammation and are less able to mount effective immune responses to new infections.

There is also evidence that an overly exuberant immune system can cause problems by directly contributing to lung damage. If the immune system gets out of control, this in itself can be dangerous and even fatal. This is why one type of therapy being tested for COVID-19 patients are drugs that dampen excessive , normally used to treat autoimmune diseases. They act by blocking the action of inflammatory protein molecules such as interleukin 6 and .

Best way out

A vaccine is the best way out. For a vaccine to really work, the critical issue is whether it can trigger the immune system enough to keep us protected for a good length of time. Nobody knows yet if this is possible.

You’ll already know that some vaccines induce immunity which lasts a lifetime, others need boosters, and some are needed annually. A lot plays into this; the rate the virus changes, whether antibodies are good at neutralising it, and so on.

For the Sars epidemic in 2002-03, also caused by a coronavirus, we think that protection lasted about a year. Other coronavirus infections tend to induce immunity for around only three months. Also, because every person’s immune system is configured slightly differently – from a combination of our genetic inheritance, the diseases we’ve previously had and any number of lifestyle factors – each person’s immunity to COVID-19 will almost certainly vary.

So much depends on our immune system: we must appreciate it more, we must step up the research, and every idea for harnessing its power must now be explored.The Conversation

, Professor of Immunology, and , Professor in Biomedical Sciences,

This article is republished from under a Creative Commons license. Read the .

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Nobel laureates among University’s most highly cited researchers /about/news/nobel-laureates-among-universitys-most-highly-cited-researchers/ /about/news/nobel-laureates-among-universitys-most-highly-cited-researchers/36815014 researchers from Vlogٷ are some of the most highly cited in their field, in a new list from the Web of Science Group released this week.

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14 researchers from are some of the most highly cited in their field, in a new list from the released this week.

They include Prof Sir Andre Geim and Prof Sir Kostya Novoselov, the co-discovers of graphene at the University in 2004, for which they won the Nobel Prize for Physics in 2010. Also on the list is fellow graphene researcher, Prof Irina Grigorieva, as well as Prof Jorgen Vestbo, a researcher in respiratory medicine, and Prof Frank Geels, and expert in energy and sustainability.

The list identifies scientists and social scientists who produced multiple papers ranking in the top 1% by citations for their field and year of publication, demonstrating significant research influence among their peers.

The methodology that determines the who’s who of influential researchers draws on the data and analysis performed by bibliometric experts from the Institute for Scientific Information at the Web of Science Group.

The data are taken from 21 broad research fields within Essential Science Indicators, a component of . The fields are defined by sets of journals and exceptionally, in the case of multidisciplinary journals such as Nature and Science, by a paper-by-paper assignment to a field based on an analysis of the cited references in the papers. This percentile-based selection method removes the citation advantage of older papers relative to recently published ones, since papers are weighed against others in the same annual cohort.

Listed University researchers;

Prof Sir Andre Geim, Dr Artem Mischenko, Prof Christian Klingenberg, Prof David Denning, Dr Donald Ward, Prof Frank Geels, Prof Irina Grigorieva, Prof Jorgen Vestbo, Prof Judith Allen, Prof Sir Kostya Novoselov, Prof Rahul Nair, Prof Richard Bardgett, Dr Roman Gorbachev, and Prof Zhiguo Ding.

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Masterswitch discovered in body’s immune system /about/news/masterswitch-discovered-in-bodys-immune-system/ /about/news/masterswitch-discovered-in-bodys-immune-system/320975Scientists have discovered a critical part of the body’s immune system with potentially major implications for the treatment of some of the most devastating diseases affecting humans.

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Scientists have discovered a critical part of the body’s immune system with potentially major implications for the treatment of some of the most devastating diseases affecting humans.

Professor Graham Lord, from Vlogٷ, led the study, which could translate into treatments for autoimmune diseases including Cancer, Diabetes, Multiple Sclerosis and Crohn’s Disease within a few years.

It is published in The Journal of Clinical Investigation today.

The discovery of the molecular pathway regulated by a tiny molecule - known as microRNA-142 - is a major advance in our understanding of the immune system.

The 10-year-study found that microRNA-142 controls Regulatory T cells, which modulate the immune system and prevent autoimmune disease. It is, they found, the most highly expressed regulator in the immune system.

Professor Lord, led the research while at Kings College London in collaboration with Professor Richard Jenner at UCL.

And according to Professor Lord, the discovery could be translated into a viable drug treatment within a few years.

He said: “Autoimmune diseases often target people in the prime of their life creating a significant socio-economic burden on them. Sometimes, the effect can be devastating, causing terrible hardship and suffering.

“But these findings represent a significant step forward in the understanding of the immune system and we believe many people worldwide may benefit.”

If the activity of Regulatory T cells is too low, this can cause other immune cells to attack our own body tissues. If these Regulatory T cells are too active, this leads to suppression of immune responses and can allow cancers to evade the immune system.

So being able to control them is a major step forward in our ability to control- and harness – the therapeutic power of the immune system.

Professor Richard Jenner from UCL, who led the computational side of the project, said that: “We were able to trace the molecular fingerprints of this molecule across other genes to determine how it acted as such a critical regulator."

Professor Lord, now Vice President and Dean of the Faculty of Biology, Medicine and Health at Vlogٷ, added: “Scientists over the past decade or so have developed therapies which are able to modulate different pathways of the immune system. We hope that this new discovery will lead to the development of new ways to treat autoimmunity, infectious diseases and cancer and we are incredibly excited about where this may lead.”

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Antibiotics are ‘avoidable trigger’ for bowel disease /about/news/antibiotics-are-avoidable-trigger-for-bowel-disease/ /about/news/antibiotics-are-avoidable-trigger-for-bowel-disease/305917Scientists at Vlogٷ have shown for the first time how antibiotics can predispose the gut to avoidable infections that trigger bowel disease in mice.

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Scientists at Vlogٷ have shown for the first time how antibiotics can predispose the gut to avoidable infections that trigger bowel disease in mice.

The team, led by , also showed that substances derived from fibre prevent this damage to the gut, suggesting a high fibre diet could be useful when taken during and after a course of antibiotics.

The research is to be published in and funded by the Wellcome Trust and the Medical Research Council.

They tested broad spectrum antibiotics on mice to assess their impact on the gut’s microbiota, the community of microbes that live in the gastrointestinal tract.

After a week long course of antibiotics, a harmful immune reaction started that lasted at least 2 months, an equivalent, say the researchers, of many years in humans.

The immune reaction meant that significantly fewer beneficial bacteria which make ‘short chain fatty acids’, which are good for the gut, grew back.

However, short chain fatty acids, produced by the fermentation of dietary fibre by the microorganisms which live in the gut, could prevent the harmful immune response.

“Epidemiological evidence already links antibiotics given to babies and young children, when the immune system is still developing, to inflammatory bowel disease, asthma, psoriasis and other inflammatory diseases later in life,” said Dr Mann, who is based at the University’s newly launched Lydia Becker Institute of Immunology and Inflammation.

She said: “However, until now it has been hard to determine cause and effect, especially with the time lag between taking the antibiotics and the development of disease later in life.

”This study helps explain the link through understanding the biological processes involved.

“Inflammatory bowel disease in particular has multiple causes but one of the triggering factors in many people has been infections such as Salmonella or E coli.

“We show that after antibiotics, mice are more susceptible to these types of infections, and do not mount the proper immune response to clear the infection.”

The gut is the largest source of bacteria in the body, where trillions of harmless bacteria critical for maintaining a healthy immune system live.

However, when antibiotics are taken orally, they deplete a massive community of bacteria in the intestines.

She added: “Not all patients taking antibiotics will get these diseases, and that’s because most people need a genetic predisposition to get them.

“And it’s very important that patients continue their antibiotics as these drugs are critical in clearing bacterial infections that can persist and cause serious health problems if left untreated.

“But what we’re saying is that antibiotics must only prescribed when absolutely needed for bacterial infections.

“Antibiotics, for example, are useless against viral infections such as those that cause the common cold, flu and many chest infections.”

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Thu, 25 Oct 2018 08:18:00 +0100 https://content.presspage.com/uploads/1369/500_electronmicroscopymousegutbacteriaandmucus.jpg?10000 https://content.presspage.com/uploads/1369/electronmicroscopymousegutbacteriaandmucus.jpg?10000
James Allison and Tasuku Honjo: deserving winners of this year's Nobel Prize in Physiology or Medicine /about/news/james-allison-and-tasuku-honjo-deserving-winners-of-this-years-nobel-prize-in-physiology-or-medicine/ /about/news/james-allison-and-tasuku-honjo-deserving-winners-of-this-years-nobel-prize-in-physiology-or-medicine/303145The 2018 Nobel Prize in Physiology or Medicine has been awarded to two immunologists for their revolutionary approaches to treat cancer. Professor Sheena Cruickshank explains the science

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The 2018 Nobel Prize in Physiology or Medicine has been awarded to two immunologists for their revolutionary approaches to treat cancer. Vlogٷ's Professor Sheena Cruickshank explains the science.

The 2018 Nobel Prize in Physiology or Medicine has been awarded to two immunologists for their revolutionary approaches to treat cancer. James Allison, based in the MD Anderson Cancer Center in Houston, Texas, and Tasuku Honjo, based at Kyoto University in Japan, led exciting and groundbreaking work on developing new types of immunotherapy that help our immune system fight cancer.

Immune cells need to be very tightly controlled to stop them being switched on inappropriately and causing inflammation. Cells in our immune system have a series of on and off switches that work in harmony to help regulate their function. The off switches – called “checkpoints” – are a bit like the brakes on your car.

This immune balancing act generally works well, but not in the case of cancer tumours. Tumours can encourage the immune brakes to stay on, which means our immune response is dampened and the immune cells cannot kill the tumour effectively.

By exploiting knowledge of how immune cells work, the researchers found that they could help the immune cells attack the tumour. The treatment works by releasing the brakes from specific immune cells called T cells. This allows the T cells to stay switched on and releases them to kill the tumour cells.

Allison was studying a protein (called CTLA-4) that is a critical brake for our immune system. It competes with our “on” switches to help control immunity. He realised that blocking CTLA-4 action could have amazing potential to help our immune cells attack tumour cells.

Honjo discovered another group of checkpoints called the PD-1 family. This family of proteins works in a completely different way to CTLA-4 but also acts as an immune brake.

Both researchers saw the potential of their work and realised that targeting these two sets of immune brakes could revolutionise cancer therapy. The discovery of checkpoint inhibitors as immunotherapy has been an enormous breakthrough in cancer therapy.

Combination therapy

A bonus is that, because these therapies have such different mechanisms, they can be used in combination. Combination therapy has proved in some cases to be even more effective at treating patient’s tumours than one drug on its own.

The field of immunotherapy is one of the most exciting fields in immunology. As we learn more about immunology and how immune cells work, we are identifying more checkpoints and more ways we can look to harness the power of our immune system to treat cancer.

Immunotherapy is also important for other diseases like autoimmunity where the immune system is overreacting. In this case, we may want to dampen the immune system to help restore the normal balance.

As we know more about immunology, the number of targets we can look to manipulate and the application of immunotherapies is growing making this an incredibly exciting time to be an immunologist.

This prize awards a fantastic body of work from two outstanding labs and is an amazing achievement. However, it is important to recognise that this groundbreaking research has been built from fundamental work on immunology and that there is a crucial place for both fundamental as well as clinically applied (so-called “translational”) work in research.The Conversation

Sheena Cruickshank, Professor in Biomedical Sciences, University of Manchester

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Image: James P. Allison and Tasuku Honjo, 2018 Nobel Laureates in Physiology or Medicine. Niklas Elmehed. Copyright: Nobel Media AB 2018

 

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