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Director
Governor
Director
Cluster Lead
Fiona Powrie FRS, FMedSci, DBE
FRS, FMedSci, DBE
Professor of Musculoskeletal Sciences and Director of the Kennedy Institute
- Dame Commander of the Most Excellent Order of the British Empire (DBE), for services to Medical Sciences
Dame Fiona Powrie is Director of the Kennedy Institute of Rheumatology and a Professor of Musculoskeletal Sciences. She leads the Mucosal Immunology research group.
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, the Louis-Jeantet Prize for Medicine 2012 and an Honorary Lifetime Membership of the British Society of Immunology in 2021.
She was elected a Fellow of the Royal Society in 2011, EMBO in 2013, the Academy of Medical Sciences in 2014 and an International Fellow of the National Academy of Sciences in 2020.
Fiona joined the Wellcome Trust Board of Governors in 2018 and was appointed Deputy Chair in 2022.
Key publications
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Circulating and Tissue-Resident CD4+ T Cells With Reactivity to Intestinal Microbiota Are Abundant in Healthy Individuals and Function Is Altered During Inflammation.
Journal article
Hegazy AN. et al, (2017), Gastroenterology, 153, 1320 - 1337.e16
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Innate lymphoid cells drive interleukin-23-dependent innate intestinal pathology.
Journal article
Buonocore S. et al, (2010), Nature, 464, 1371 - 1375
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Intestinal homeostasis and its breakdown in inflammatory bowel disease.
Journal article
Maloy KJ. and Powrie F., (2011), Nature, 474, 298 - 306
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The alarmin IL-33 promotes regulatory T-cell function in the intestine.
Journal article
Schiering C. et al, (2014), Nature, 513, 564 - 568
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Innate lymphoid cells sustain colon cancer through production of interleukin-22 in a mouse model.
Journal article
Kirchberger S. et al, (2013), J Exp Med, 210, 917 - 931
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A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages.
Journal article
Danne C. et al, (2017), Cell Host Microbe, 22, 733 - 745.e5
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Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor-neutralizing therapy in patients with inflammatory bowel disease.
Journal article
West NR. et al, (2017), Nat Med, 23, 579 - 589
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Defining the microbial transcriptional response to colitis through integrated host and microbiome profiling.
Journal article
Ilott NE. et al, (2016), ISME J, 10, 2389 - 2404
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Granulocyte Macrophage Colony-Stimulating Factor-Activated Eosinophils Promote Interleukin-23 Driven Chronic Colitis.
Journal article
Griseri T. et al, (2015), Immunity, 43, 187 - 199
Recent publications
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MHC class II antigen presentation by intestinal epithelial cells fine-tunes bacteria-reactive CD4 T-cell responses.
Journal article
Heuberger CE. et al, (2024), Mucosal Immunol, 17, 416 - 430
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Elevated type-17 cytokines are present in Axial Spondyloarthritis stool
Journal article
BOWNESS P. and BROUGH I., (2024), Discovery Immunology
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Blimp-1 and c-Maf regulate immune gene networks to protect against distinct pathways of pathobiont-induced colitis.
Journal article
Alvarez-Martinez M. et al, (2024), Nat Immunol
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Immune microniches shape intestinal Treg function.
Journal article
Gu Y. et al, (2024), Nature
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Alterations in the gut microbiome implicate key taxa and metabolic pathways across inflammatory arthritis phenotypes.
Journal article
Thompson KN. et al, (2023), Sci Transl Med, 15