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 remodelling and repair - 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.
Byrne AJ. et al, (2016), Mucosal Immunol
Distinct microenvironmental cues stimulate divergent TLR4-mediated signaling pathways in macrophages.
Piccinini AM. et al, (2016), Sci Signal, 9
Udalova IA. et al, (2016), Nat Rev Rheumatol, 12, 472 - 485
Targeted IL-4 therapy synergizes with dexamethasone to induce a state of tolerance by promoting Treg cells and macrophages in mice with arthritis.
Kawalkowska JZ. et al, (2016), Eur J Immunol, 46, 1246 - 1257
Dynamic spatio-temporal contribution of single β5t+ cortical epithelial precursors to the thymus medulla.
Mayer CE. et al, (2016), Eur J Immunol, 46, 846 - 856
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
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