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Meeting report

Kennedy Institute of Rheumatology Division, Imperial College London, 12–13 November 2003: Towards a molecular toolkit for studying lymphocyte function in inflammatory arthritis

Jeff Faint1* and Frances Hall2

Author Affiliations

1 The University of Birmingham/MRC Centre for Immune Regulation, University of Birmingham, Birmingham, UK

2 University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, UK

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Arthritis Res Ther 2004, 6:55-59  doi:10.1186/ar1162

Published: 8 March 2004

Abstract

T lymphocytes have been implicated in the pathogenesis of inflammatory arthritis for approximately 30 years. Over that period a vast literature has described the phenotype, location and behaviour of T cells derived from patients with inflammatory rheumatological disease. The arthritiogenic roles of MHC class I and class II molecules, which present antigen to T cells, have been hotly debated. The T cell has been variously conceived as a central or peripheral (or even incidental) component in the arthritogenic response. Rapid developments in genomics and use of biological therapeutic agents coupled with recent insights in the field of T cell differentiation and immunoregulation together offer novel methods of investigating the pathogenesis of chronic inflammatory disease. A number of UK researchers, with diverse interests within the field of synovitis, met recently at the Kennedy Institute of Rheumatology. Presentations on T cell memory, cytokines of homeostasis and inflammation, unconventional behaviour of MHC molecules and immunoregulation in murine models, rheumatoid and spondyloarthritis reflected the breadth of the discussion.

Keywords:
cytokines; HLA-B27; immunoregulation; migration; rheumatoid arthritis; spondyloarthritis