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Open Access

Genetics of Rheumatoid Arthritis

  • Gerald T Nepom1
Arthritis Research & Therapy19991(Suppl 1):S01

https://doi.org/10.1186/ar15

Published: 15 November 1999

Keywords

PeptideRheumatoid ArthritisSusceptibility GeneBinding MotifCell Contact

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.

Authors’ Affiliations

(1)
Virginia Mason Research Center, Seattle, USA

References

  1. Nepom GT: Major histocompatibility complex-directed susceptibility to rheumatoid arthritis. Adv Immunol. 1998, 68: 315-332.PubMedView ArticleGoogle Scholar

Copyright

© Current Science Ltd 2000

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