Kennedy Institute of Rheumatology
We are a world-leading basic and translational inflammatory sciences centre. The three major themes of our research - immunity and microbiome, 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.
Krausgruber T. et al, (2016), Nat Commun, 7
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
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
Our Arthritis Research UK Centre of Excellence aims to develop new treatments for arthritis, improving healthcare and transforming people's lives.
IRF5 REGULATES ALLERGIC AIRWAY INFLAMMATION
The pulmonary immune system protects the host from infection but also drives chronic allergic diseases such as asthma. The Udalova lab show in Mucosal Immunology that transcription factor IRF5 promotes effective responses to inhaled antigen and that IRF5-deficient macrophages drive airway hyperreactivity. Read full paper.
INJURY-INDUCED MACROPHAGE TLR4 RESPONSES
Both bacterial LPS and tissue damage-associated Tenascin-C activate TLR4 signalling in macrophages. The Midwood lab show in Science Signaling that although these ligands activate some common pathways, LPS-stimulated macrophages are biased toward matrix destruction whereas tenascin-C-stimulated macrophage synthesise matrix components. Read full paper.