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This article is part of the supplement: Fourth International Synovitis Workshop

Meeting abstract

Genetics of Rheumatoid Arthritis

Gerald T Nepom

  • Correspondence: Gerald T Nepom

Author Affiliations

Virginia Mason Research Center, Seattle, Washington, USA

Arthritis Res 2000, 1(Suppl 1):S01-332  doi:10.1186/ar15

The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/15nov99/ar01s1


Published:15 November 1999

© 2000 Current Science Ltd

Full text

Genetic associations between rheumatoid arthritis and specific HLA class II genes provide clues to understanding the molecular basis for disease susceptibility. There is a remarkable structural relationship among different rheumatoid arthritis (RA) susceptibility genes, in which each of the associated class II alleles encodes a sequence of key amino acids termed the `shared epitope.' Mechanistic models to account for the shared epitope association with RA can be interpreted in the context of an HLA-directed pathway for the development of disease. We suggest that altered T cell activation results from recognition of the shared epitope, providing a potential mechanism by which the shared epitope may be involved in the generation or modulation of self-recognition during antigen presentation and processing. We propose that the shared epitope association with RA is not solely based on a specific peptide binding motif and peptide determinant selection but rather is influenced by a strongly biased direct recognition of shared epitope residues by direct T cell contact.

References

  1. Nepom GT: Major histocompatibility complex-directed susceptibility to rheumatoid arthritis.

    Adv Immunol 1998, 68:315-332. PubMed Abstract OpenURL