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.”

The University of Manchester 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 The University of Manchester, 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

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 The University of Manchester 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

Grace Harvey, also came 6^th 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 91ֱ�� 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.

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 26^th August and the 100m breastroke on day 4, the 28^th 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 91ֱ�� 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. 

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 The University of Manchester, 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.”

In The Secret Body published by Vintage Books, Professor Dan Davis from The University of Manchester 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.”

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

Led by University of Manchester scientists at the Cancer Research UK 91ֱ�� 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 91ֱ��, 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 The University of Manchester.

“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

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 91ֱ�� 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.

91ֱ�� author Dr Joanne Konkel from The University of Manchester 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.

91ֱ�� author Dr Madhvi Menon from The University of Manchester 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.

91ֱ�� author Dr John Grainger from The University of Manchester 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

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 91ֱ�� 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 91ֱ��.

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 The University of Manchester 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

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 91ֱ�� 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 The University of Manchester and Consultant in Paediatric Immunology Royal 91ֱ�� 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.

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 The University of Manchester.

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 91ֱ�� 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 91ֱ�� and 91ֱ�� 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 

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 The University of Manchester 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 The University of Manchester. 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.

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.

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 The University of Manchester, 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 The University of Manchester, 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.”

Scientists at The University of Manchester 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.”

The 2018 Nobel Prize in Physiology or Medicine has been awarded to two immunologists for their revolutionary approaches to treat cancer. The University of Manchester'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