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