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Ann Rheum Dis 2000;59:497-499 ( July )

Leader

Rheumatoid arthritis and Epstein-Barr virus: a case of living with the enemy?

The first 150 words of the full text of this article appear below.

    Article

The cause of rheumatoid arthritis (RA) still eludes us, though we know from twin studies that both genetic and environmental factors are important contributory components to disease susceptibility1; the latter is estimated to account for about one half of this risk.2 At least one major RA susceptibility gene resides within the major histocompatibility complex (MHC) region. Current dogma is that this is explained by a conserved sequence of amino acids within the third hypervariable region of the DRB1 beta  chain molecule encoded by a number of alleles. This is usually referred to as being the RA shared epitope hypothesis.3 Although DRB1 molecules present peptide fragments to T cell receptors on CD4 positive lymphocytes, the exact mechanism through which the RA shared epitope exerts its effect remains unclear.4 Given that class II molecules such as DRB1 serve an immunoregulatory role, it is not surprising that polymorphisms within these structures will influence . . . [Full text of this article]




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