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  • Meeting abstract
  • Open Access

Genetics of Rheumatoid Arthritis

  • 1
Arthritis Research & Therapy19991 (Suppl 1) :S01

https://doi.org/10.1186/ar15

  • Published:

Keywords

  • Peptide
  • Rheumatoid Arthritis
  • Susceptibility Gene
  • Binding Motif
  • Cell 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, Washington, USA

References

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

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