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Commentary

Altered signalling thresholds in T lymphocytes cause autoimmune arthritis

Andrew P Cope

Author Affiliations

Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College, London, UK

Arthritis Res Ther 2004, 6:112-116  doi:10.1186/ar1185

Published: 23 April 2004

Abstract

The development of spontaneous autoimmunity in inbred strains of rodents has allowed us to investigate the molecular basis of chronic inflammatory disease in ways that would not be possible in humans. Recently, two new mouse models of autoimmune inflammatory polyarthritis have been reported that demonstrate how alterations in signalling thresholds sufficient to perturb central T-cell tolerance lead to inflammatory arthritis. These mice provide new insights into the complexities of what may turn out to be a heterogeneous group of diseases that we call rheumatoid arthritis. They will also provide unique tools for dissecting precisely how chronically activated T cells contribute to the effector phase of arthritis through mechanisms that may be less dependent on antigen receptor signalling.

Keywords:
autoimmune arthritis; signalling; T cells; thymic selection