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Rheumatology 2002; 41: 1341-1345
© 2002 British Society for Rheumatology

Editorial

Unmasking the anti-inflammatory cytokine response in rheumatoid synovitis

R. Gerli, C. Lunardi1 and C. Pitzalis2

Department of Clinical and Experimental Medicine, Section of Internal Medicine and Oncological Sciences, Center for the Study of Rheumatic Diseases, University of Perugia, Perugia,
1 Department of Clinical and Experimental Medicine, Section of Internal Medicine, University of Verona, Verona, Italy and
2 Department of Rheumatology, Division of Medicine, Guy's and St Thomas' School of Medicine (GKT), Guy's Campus, London, UK

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The contribution of T lymphocytes to the pathogenesis of rheumatoid arthritis (RA) remains a matter of intense debate. Few people, however, would question the central role of T cells in initiating and modulating RA immune pathogenesis via the recognition of some unknown (exogenous/auto-)antigens in the joint and the production of various cytokines [1–3]. In this regard, there is general agreement that RA synovitis is a Th1-dominated disease [4]. Th1 cells, indeed, are prominent among the T cells isolated from the synovium of patients with RA [5–7]. In addition, T-cell clones from the rheumatoid joint produce predominantly proinflammatory cytokines, such as interleukin (IL)-2, interferon (IFN)-{gamma} and IL-12 [8, 9]. Selective enrichment of Th1 cells in the RA synovium is also suggested by single-cell analysis of synovial CD4+ T cells that demonstrates greater production of the Th1 cytokine IFN-{gamma} . . . [Full Text of this Article]


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