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Logo of arthrestherBioMed Centralbiomed central web sitesearchsubmit a manuscriptregisterthis articleArthritis Research & Therapy
Arthritis Res Ther. 2004; 6(3): 112–116.
Published online Apr 23, 2004. doi:  10.1186/ar1185
PMCID: PMC416454
Altered signalling thresholds in T lymphocytes cause autoimmune arthritis
Andrew P Copecorresponding author1
1Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College, London, UK
corresponding authorCorresponding author.
Andrew P Cope: andrew.cope/at/
Received February 25, 2004; Revisions requested April 2, 2004; Revised April 5, 2004; Accepted April 7, 2004.
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
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