The mechanism underlying the effect of the shared epitope is unclear, but it was postulated that the presentation of arthritogenic self-peptides, molecular mimicry with foreign antigens or T cell repertoire selection are involved. While these hypotheses are all plausible, they are difficult to reconcile with the fact that data supporting antigen-specific responses as the primary event in reumathoid arthritis are inconclusive. Additionally, several other human disease have also been shown to be associated with shared epitope encoding DRB1 alleles such as type I diabetes, systemic lupus erythemathosus and autoimmune hepatitis.
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