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

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

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	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  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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