MOLECULAR MIMICRY - CAN EPITOPE MIMICRY INDUCE AUTOIMMUNE-DISEASE

Mimicry of host antigens by infectious agents may induce cross-reactiv e autoimmune responses to epitopes within host proteins which, in susc eptible individuals, may tip the balance of immunological response ver sus tolerance toward response and subsequently lead to autoimmune dise ase. Epitope mimicry may indeed be involved in the pathogenesis of sev eral diseases such as post-viral myocarditis or Chagas disease. but fo r many other diseases in which it has been implicated, such as insulin -dependent diabetes mellitis or rheumatoid arthritis, convincing evide nce is still lacking. Even if an epitope mimic can support a cross-rea ctive T or B cell response in vitro, its ability to induce an autoimmu ne disease in vivo will depend upon the appropriate presentation of th e mimicked host antigen in the target tissue and, in the case of T cel l mimics, the ability of the mimicking epitope to induce a proliferati ve rather than anergizing response upon engagement of the MHC-peptide complex with the T cell receptor. B cell presentation of mimicking for eign antigen to T cells is a possible mechanism for instigating an aut oimmune response to self antigens that in turn can lead to autoimmune disease under particular conditions of antigen presentation, secondary signalling and effector cell repertoire. In this review evidence in s upport of epitope mimicry is examined in the light of the necessary im munological considerations of the theory.