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Annu Rev Pathol. 2009;4:417-34. doi: 10.1146/annurev.pathol.4.110807.092254.

The immunopathogenesis of rheumatoid arthritis.

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1
Department of Medicine, University of California, and Division of Rheumatology, San Francisco General Hospital, San Francisco, CA 94110, USA. jimboden@medsfgh.ucsf.edu

Abstract

Rheumatoid arthritis is a chronic inflammatory polyarthritis whose etiology remains uncertain. Recently we have learned that autoimmunity to citrullinated protein antigens has specificity for rheumatoid arthritis and defines a clinically and genetically distinct form of the disease. Multiple genes contribute to disease susceptibility, with the HLA locus accounting for 30% to 50% of overall genetic risk. Five risk loci have been identified and validated: HLA-DRB1, PTPN22, STAT4, a region in 6q23, and the TRAF1/C5 locus. Also, there is renewed interest in the contribution of T cells to ongoing inflammation in rheumatoid arthritis. Autoantibodies to citrullinated protein epitopes are specific for rheumatoid arthritis, are associated with a more aggressive disease course, and are pathogenic in an animal model of autoimmune arthritis. There is a strong association between shared-epitope-expressing HLA-DRB1 alleles and the development of rheumatoid arthritis associated with autoimmunity to citrullinated protein antigens.

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