Fiona Powrie FRS

FMedSci

Professor of Musculoskeletal Sciences and Director of the Kennedy Institute

Principal Investigator in the Translational Gastroenterology Unit, University of Oxford

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.

Key publications

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
Innate lymphoid cells drive interleukin-23-dependent innate intestinal pathology.
Journal article

Buonocore S. et al, (2010), Nature, 464, 1371 - 1375
Intestinal homeostasis and its breakdown in inflammatory bowel disease.
Journal article

Maloy KJ. and Powrie F., (2011), Nature, 474, 298 - 306
The alarmin IL-33 promotes regulatory T-cell function in the intestine.
Journal article

Schiering C. et al, (2014), Nature, 513, 564 - 568
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
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
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
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
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

The interleukin 22 pathway interacts with mutant KRAS to promote poor prognosis in colon cancer.
Journal article

McCuaig S. et al, (2020), Clin cancer res
Correction: Defining the microbial transcriptional response to colitis through integrated host and microbiome profiling.
Journal article

Ilott NE. et al, (2020), Isme j, 14
Loss of IL-10 signaling in macrophages limits bacterial killing driven by prostaglandin E2.
Journal article

Mukhopadhyay S. et al, (2020), J exp med, 217
High-throughput phenotyping reveals expansive genetic and structural underpinnings of immune variation.
Journal article

Abeler-Dörner L. et al, (2020), Nat immunol, 21, 86 - 100
Very Early Onset Inflammatory Bowel Disease: A Clinical Approach With a Focus on the Role of Genetics and Underlying Immune Deficiencies.
Journal article

Ouahed J. et al, (2019), Inflamm bowel dis

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