Kennedy Institute of Rheumatology
We are a world-leading basic and translational inflammatory sciences centre. The three major themes of our research - immunology, inflammation biology, and tissue repair and regeneration - are relevant for a diverse range of chronic inflammatory disorders, including arthritis, inflammatory bowel disease, tissue fibrosis and certain types of cancer. We apply state-of-the-art technologies in analysis of disease models and patient tissue samples to understand why disease develops and to reveal new diagnostic markers and targets for therapy. Strategic partnerships with nearby clinical centres such as the Nuffield Orthopaedic Centre and the John Radcliffe Hospital facilitate scientific translation from bench to bedside.
CD11c(+) monocyte/macrophages promote chronic Helicobacter hepaticus-induced intestinal inflammation through the production of IL-23.
Arnold IC. et al, (2016), Mucosal Immunol, 9, 352 - 363
Selective Inhibition of Membrane Type 1 Matrix Metalloproteinase Abrogates Progression of Experimental Inflammatory Arthritis: Synergy With Tumor Necrosis Factor Blockade.
Kaneko K. et al, (2016), Arthritis Rheumatol, 68, 521 - 531
Indoleamine 2,3-dioxygenase-1 is protective in atherosclerosis and its metabolites provide new opportunities for drug development.
Cole JE. et al, (2015), Proc Natl Acad Sci U S A, 112, 13033 - 13038
Actin foci facilitate activation of the phospholipase C-γ in primary T lymphocytes via the WASP pathway.
Kumari S. et al, (2015), Elife, 4
Our Arthritis Research UK Centre of Excellence aims to develop new treatments for arthritis, improving healthcare and transforming people's lives.
immunological synapse explained
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DRIVERS OF DYSBIOSIS IN COLITIS
In a paper published in ISME, the Powrie Lab use combined metagenomic and metatranscriptomic sequencing to profile the gut microbiota in colitis. They find increased abundance and transcription of microbial gene families involved in oxidative stress resistance, rare nutrient uptake and defence against antimicrobial peptides. These findings suggest that in colitis environmental stressors in the inflamed gut drive dysbiosis. Full paper
IDO ENZYME PROTECTS IN ATHEROSCLEROSIS
The enzyme indoleamine-2,3-dioxygenase (IDO) catalyses degradation of the essential amino acid tryptophan into immunomodulatory metabolites. The Monaco lab report in PNAS that IDO metabolites stimulate B cell interleukin-10 production and are protective in atherosclerosis. Full paper