Immunology of the exposome: addressing the crisis in chronic inflammatory disease

12 - 13 October 2026 09:00 - 17:00 The Royal Society Free Watch online
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Discussion meeting organised by Professor Judith Allen FMedSci FRS and Dame Fiona Powrie DBE FMedSci FRS

Exposure to environmental challenges such as pollutants and infections (collectively the exposome) interact with our genes to cause and exacerbate chronic inflammatory diseases. However, we do not understand how the immune system at barrier surfaces decodes environmental drivers of disease. By bringing together immunologists with environmental scientists we aim to drive new solutions to the global crisis of chronic disease.

Programme

The programme, including speaker biographies and abstracts, will be available soon. Please note that the programme may be subject to change.

Poster session

There will be a poster session on Monday 12 October 2026. If you would like to present a poster, please submit your proposed title, abstract (up to 200 words), author list, and the name of the proposed presenter and institution no later than Friday 11 September 2026. Acceptances may be made on a rolling basis so we recommend submitting as soon as possible in case the session becomes full. Submissions made within one month of the meeting may not be included in the programme booklet.

Attending the event

This event is intended for researchers in relevant fields.

  • Free to attend
  • Both virtual and in-person attendance is available. Advance registration is essential
  • Lunch is available on both days of the meeting for an optional £25 per day. There are plenty of places to eat nearby if you would prefer to purchase food offsite. Participants are welcome to bring their own lunch to the meeting

Please note that scientific meetings hosted by the Royal Society do not necessarily represent a Royal Society position or signify an endorsement of the speakers or content presented.

Enquiries: Contact the Scientific Programmes team.

Organisers

  • Professor Dame Fiona Powrie DBE FMedSci FRS

    Professor Dame Fiona Powrie DBE FMedSci FRS

    Fiona Powrie is the Director of the Kennedy Institute of Rheumatology and Principal Investigator in the Translational Gastroenterology Unit, University of Oxford. Her research interests include characterisation of the interaction between the intestinal microbiota and the host immune system and how this mutualistic relationship breaks down in inflammatory bowel disease.

    Fiona's work has identified the functional role of regulatory T cells in intestinal homeostasis and shed light on their development and mechanism of action. She has also shown that both adaptive and innate immune mechanisms contribute to intestinal inflammation and identified the IL-23 pathway as a pivotal player in the pathogenesis of chronic intestinal inflammation.

    Her current work seeks to translate findings from model systems into the clinic in inflammatory bowel disease patients. Fiona received the Ita Askonas Award from the European Federation of Immunological Societies for her contribution to immunology in Europe and the Louis-Jeantet Prize for Medicine 2012.

    She was elected a Fellow of the Royal Society in 2011, EMBO in 2013 and the Academy of Medical Sciences in 2014. Fiona joined the Wellcome Trust's Board of Governors in 2018.

  • Professor Judith Allen FMedSci FRS

    Professor Judith Allen FMedSci FRS

    Judi Allen has a PhD from the University of California, Berkeley. Following a postdoc at Imperial College, London, she established her own group at the University of Edinburgh. In 2016 Judi moved to the University of Manchester, where she is currently a Professor of Immunobiology in the Lydia Becker Institute of Immunology & Inflammation and the Manchester Cell Matrix Centre, and Director of the MRC CoRE in Exposome Immunology. The Allen laboratory investigates the host immune response to parasite infection with a focus on type 2 immunity, the response mammals characteristically make to large multicellular parasites (helminths). Her studies of macrophage function in type 2 settings led to an increased understanding of the evolutionary relationship between type 2 immunity, parasite control and tissue repair. Her lab is currently investigating how the type 2 cytokines, IL-4 and IL-13, regulate the extra-cellular matrix.

Schedule

Chair

Professor Judith Allen FMedSci FRS

Professor Judith Allen FMedSci FRS

University of Manchester, UK

09:00-09:05 Welcome by the Royal Society and organiser
Professor Judith Allen FMedSci FRS

Professor Judith Allen FMedSci FRS

University of Manchester, UK

09:05-09:35 Talk title TBC
Professor Martine Vrijheid

Professor Martine Vrijheid

Barcelona Institute for Global Health, Spain

09:35-10:00 Human immune systems are shaped by environmental exposures early in life
Dr Petter Brodin

Dr Petter Brodin

Imperial College London, UK

10:00-10:30 Talk title TBC
Dr Darragh Duffy

Dr Darragh Duffy

Pasteur Institute, France

10:30-11:00 Talk title TBC
Professor Magnus Rattray

Professor Magnus Rattray

University of Manchester, UK

11:00-11:15 Coffee break
11:15-11:45 UK Biobank: scale, depth, duration… but, most importantly, accessibility

With its unique combination of scale, depth, duration and accessibility, UK Biobank is enabling tens of thousands of researchers worldwide to perform innovative discovery science. This talk will provide information about UK Biobank and highlight recent enhancements.

UK Biobank is a prospective cohort study of 500,000 people aged 40-69 years when recruited from across the United Kingdom in 2006-10. It integrates large-scale genomic data (including sequencing) and deep phenotyping data (including lifestyle factors, physical measures and multi-modal imaging) with long-term longitudinal health records. The recent addition of large-scale proteomic and metabolomic data has created an even more powerful resource for enabling better understanding of disease biology and discovery of novel drug targets.

In order to accommodate the increasing scale and complexity of the database, UK Biobank has established a cloud-based Research Analysis Platform. It provides secure access to large-scale computing and novel technologies without the problems of transferring, collating, storing, and accessing these large-scale data. The provision of financial credits for early-career researchers and those in less well-resourced settings democratises access to this unique research resource, further enabling advances in discovery science and improvements in human health.

Sir Rory Edwards Collins FMedSci FRS

Sir Rory Edwards Collins FMedSci FRS

UK Biobank

11:45-12:15 Discussion: Tools to interrogate cohort data

Chair

Professor Sheena Cruickshank

Dr Sheena Cruickshank

University of Manchester, UK

13:30-13:50 Talk title TBC
Dr Gyaviira Nkurunungi

Dr Gyaviira Nkurunungi

MRC/UVRI and LSHTM Uganda Research Unit, Uganda and LSHTM, UK

13:50-14:10 Talk title TBC
14:10-14:30 Talk title TBC
14:30-15:00 Discussion
Dr Sheena Cruickshank

Dr Sheena Cruickshank

University of Manchester, UK

15:00-15:30 Coffee break
15:30-15:50 Measuring air pollution and human exposure

Measuring human exposure to air pollution creates a technical and data analysis challenge. The UK has a relatively extensive outdoor air pollution measurement network (~300 sites), but even this is hampered by the relatively small number of species measured and the differing representativeness of the measurement locations. Over the past five years, three urban ‘supersites’ have been created that augment the network with measurements of a wide range of other species, enabling a greater assessment of human exposure to poor air quality in the urban environment. Such measurements can be complemented with high resolution satellite measurements to provide a greater spatial coverage for targeted pollutants.

However, as we spend 90% of our time indoors, we must consider air quality within the home and workplace that might be different from outdoors both in terms of concentrations and also chemical composition. This creates even more of a challenge as every building is different and it is often inconvenient to deploy the necessary instrumentation in people's homes. Advancements in lower-cost/miniaturised sensor technologies have enabled the development of highly portable instrumentation suitable for the assessment of personal exposure to multiple pollutants. This enables us to draw more reliable associations between exposure and health effects in panels of hundreds of people.

Professor James Lee

Professor James Lee

York University, UK

15:50-16:10 Talk title TBC
16:10-16:30 Talk title TBC
16:30-17:00 Discussion and closing remarks

Chair

Professor Dame Fiona Powrie DBE FMedSci FRS

Professor Dame Fiona Powrie DBE FMedSci FRS

University of Oxford, UK

09:00-09:30 Asthma as a disease of impaired barrier function

Asthma is an inflammatory disorder of the airways of reduced regulatory T cell-induced tolerance leading to induction of T(H)2- and innate ILC2-type lymphocytes, IgE-driven mast cell activation and eosinophil recruitment and driven by a cytokine gene cluster on 5q31-q33 encoding interleukin-4 (IL-4), -5, -9, -13 and GM-CSF. Interrupting this cascade forms the basis of modern asthma treatment with allergen immunotherapy, topical corticosteroids and IgE/cytokine blocking biologics.

Upstream of the T2 inflammatory cascade is the epithelium which orchestrates the inflammatory response by interacting with environmental allergens, microbes and pollutants to produce a chronic wound scenario involving tissue injury and aberrant repair. Epithelial cells become active responders to these environmental threats through structural damage, barrier failure and abnormal repair leading to chronic inflammation and remodelling manifesting as goblet cell hyperplasia, matrix deposition and an increase in smooth muscle.

Four interacting processes are involved: 1) Breakdown in barrier function results from disruption of epithelial cell tight junctions allowing inhaled substances to pass more easily into the airway wall and interact with immune and inflammatory cells, 2) Release of alarmins (eg, TSLP, IL-33, IL-25, adenosine) from injured airway epithelial cells to trigger T2 and ILC2 effector responses, 3) Generation of growth factors to promote remodelling and persistent inflammatory phenotypes and 4) Reduced mucosal anti-oxidant defence and innate immunity to enhance susceptibility to air pollutants and respiratory viruses. The "epithelial era" of research emphases the epithelium as a primary target for treatment (eg, anti-TSLP) to prevent initiation of the inflammatory cascade at its source.

Professor Sir Stephen Holgate CBE KBE FMedSci

Professor Sir Stephen Holgate CBE KBE FMedSci

University of Southampton, UK

09:30-10:00 Talk title TBC
Professor Anna Hansell

Professor Anna Hansell

University of Leicester, UK

10:00-10:30 Talk title TBC
Dr James Lee

Dr James Lee

The Francis Crick Institute, UK

10:30-11:00 Coffee break
11:00-11:30 Talk title TBC
11:30-12:00 Talk title TBC
12:00-12:30 Talk title TBC

13:30-14:00 Talk title TBC
Dr Suzanne Cloonan

Dr Suzanne Cloonan

Trinity College Dublin, Ireland

14:00-14:30 Talk title TBC
14:30-15:00 Outside the brain: how glial cells orchestrate tissue immunity

Inflammatory diseases of the gut, lung and skin are major contributors to global morbidity and mortality. While epithelial, immune and stromal cell interactions have been extensively studied, treatment options remain limited. Identifying previously unrecognised cellular regulators of tissue immunity is therefore an urgent clinical priority.

Our recent work has uncovered unexpected immunoregulatory roles for enteric glial cells. Using transcriptomic profiling and gene knockout models, we identified an IFNγ-enteric glia signalling axis that is essential for maintaining intestinal immune homeostasis and tissue integrity at steady state. Activation of this pathway is also required for effective tissue repair following pathogen invasion. Developmental lineage analysis further revealed tissue context-dependent immune gene modules in enteric glia, highlighting their broader immunological potential.

Using spatial transcriptomics, we demonstrate that enteric glia form transcriptionally distinct, spatially organised communities that shape intestinal architecture in health and disease. We show that the intestine is compartmentalised, with the muscularis externa, which houses enteric ganglia, representing a region relatively shielded from immune infiltration. In Crohn’s disease, however, inflammatory glial populations emerge within the muscularis adjacent to immune cell infiltrates. Mechanistically, gene knockout model reveals that enteric glia drive intestinal plexitis by upregulating chemokines within this compartment. Together, these findings redefine enteric glia as central regulators of immune compartmentalisation and tissue defence in the intestine, providing a new conceptual framework for understanding neuro-immune interactions across barrier tissues and highlighting glial networks as potential therapeutic targets in chronic inflammatory disease.

Dr Fränze Progatzky

Dr Fränze Progatzky

Oxford University, UK

15:00-15:30 Coffee break
15:30-16:00 Talk title TBC
16:00-16:45 Discussion
16:45-17:00 Overview and closing remarks
Professor Judith Allen FMedSci FRS

Professor Judith Allen FMedSci FRS

University of Manchester, UK

Professor Dame Fiona Powrie DBE FMedSci FRS

Professor Dame Fiona Powrie DBE FMedSci FRS

University of Oxford, UK