Key Publications
Thomas et al. A longitudinal single-cell atlas of anti-tumour necrosis factor treatment in inflammatory bowel disease. Nature Immunology 2024; epub 22/10.2024.
Friedrich M & Pohin M & Jackson MA et al. IL-1-driven stromal-neutrophil interaction in deep ulcers identifies a pathotype of therapy non-responsive inflammatory bowel disease patients. Nature Medicine 2021; 27: 1970.
Friedrich M & Travis S. Shining a Light on Barrier Function. Gastroenterology 2023; 164(2):184.
Friedrich M & Pohin M & Powrie F. Cytokine Networks in the Pathophysiology of Inflammatory Bowel Disease. Immunity 2019; 50:992.
West N & Hegazy A. et al. Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor–neutralizing therapy in patients with inflammatory bowel disease. Nature Medicine 2017; 23:579.
Korsunsky I & Wei K & Pohin M & Kim EY & Barone F. Cross-tissue, single-cell stromal atlas identifies shared pathological fibroblast phenotypes in four chronic inflammatory diseases. Med 2022; 3(7): 481.
Hackstein CP et al. A conserved population of MHC II-restricted, innate-like, commensal-reactive T cells in the gut of humans and mice. Nature Communications 2022; 13(1):7472.
Tillack C & Ehmann LM & Friedrich M et al. Anti-TNF antibody-induced psoriasiform skin lesions in patients with inflammatory bowel disease are characterised by interferon-γ-expressing Th1 cells and IL-17A/IL-22-expressing Th17 cells and respond to anti-IL-12/IL-23 antibody treatment. Gut 2014; 63:567.
Friedrich M et al. Intestinal neuroendocrine cells and goblet cells are mediators of IL-17A-amplified epithelial IL-17C production in human inflammatory bowel disease. Mucosal Immunology 2015; 8:943.
Demetriou P et al. A dynamic CD2-rich compartment at the outer edge of the immunological synapse boosts and integrates signals. Nature Immunology 2020; 21:1232.
Research groups
Matthias Friedrich
Dr. rer. biol. hum.
Group Leader (Wellcome Trust Career Development Award)
Gastrointestinal Pathophysiology - Translational Research and Experimental Medicine
Research
Our team is interested in the cellular and molecular mechanisms of chronic inflammation and fibrosis. Whilst the focus is on Inflammatory Bowel Diseases (IBDs), we aim to identify shared and distinct patho-mechanisms across organs. Combining cutting edge digital pathology and AI approaches, spatial/single-cell/bulk genomics and proteomics, highly multiplexed immunohistochemistry and flow cytometry, we profile large patient cohorts. This is complemented by mechanistic studies of in vivo disease models and in vitro organotypic tissue cultures. Current projects strive to personalise medical therapy in IBD, finding alternative treatments for fibrotic Crohn's disease, and establishing a molecular basis for symptoms in ulcerative colitis.
Team
Research Assistants:
Osheen Sharma
Laboratory and Administrative Assistants:
Kate Hutton
Postdocs:
Hosuk Ryou (co-supervised)
Kristina Clark (Academic Clinical Lecturer, co-supervised)
DPhil students:
Zhi Wong (co-supervised)
Julia Pakpoor (co-supervised)
Tom Hosack (co-supervised)
Clinical Fellows:
Khalid Shamiyah
Former lab members:
Kaiyang Song
Rahul Ravindran
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, (2023), Mucosal Immunology
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Adipocyte autophagy limits gut inflammation by controlling oxylipin and IL‐10
Journal article
Richter FC. et al, (2023), The EMBO Journal, 42
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MHC class II antigen presentation by intestinal epithelial cells fine-tunes bacteria-reactive CD4 T cell responses
Preprint
Heuberger CE. et al, (2023)
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Systemic and T cell-associated responses to SARS-CoV-2 immunisation in gut inflammation (STAR SIGN study): effects of biologics on vaccination efficacy of the third dose of mRNA vaccines against SARS-CoV-2.
Journal article
Woelfel S. et al, (2023), Alimentary pharmacology & therapeutics, 57, 103 - 116
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Anti-TNF-induced IL-27 modulates regulatory T cell responses in patients with IBD that respond to therapy
Preprint
Peres RS. et al, (2022)