Kennedy Institute of Rheumatology
We are a world-renowned centre of excellence in immunology and inflammation research, from bench to bedside.
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
Granulocyte Macrophage Colony-Stimulating Factor-Activated Eosinophils Promote Interleukin-23 Driven Chronic Colitis.
Griseri T. et al, (2015), Immunity, 43, 187 - 199
Weiss M. et al, (2015), Proc Natl Acad Sci U S A, 112, 11001 - 11006
Our Arthritis Research UK Centre of Excellence aims to develop new treatments for arthritis, improving healthcare and transforming people's lives.
ILC3S ORCHESTRATE GUT INFLAMMATION
Innate lymphoid cells (ILC) accumulate in the inflamed intestine in inflammatory bowel disease (IBD), but how this relatively sparse population of cells could promote dramatic inflammation in the gut has been unclear. The Powrie Lab show in Elife that group 3 ILC produce the inflammatory cytokine GM-CSF that recruits additional inflammatory cell types to exacerbate IBD. Full paper
IDO ENZIME 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