Molecular mimicry: Can epitope mimicry induce autoimmune disease?

Davies, J. M. (1997) Molecular mimicry: Can epitope mimicry induce autoimmune disease? Immunology and Cell Biology, 75(2), pp. 113-126.

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Abstract

Mimicry of host antigens by infectious agents may induce cross-reactive autoimmune responses to epitopes within host proteins which, in susceptible individuals, may tip the balance of immunological response versus tolerance toward response and subsequently lead to autoimmune disease. Epitope mimicry may indeed be involved in the pathogenesis of several diseases such as post-viral myocarditis or Chagas disease, but for many other diseases in which it has been implicated, such as insulin-dependent diabetes mellitis or rheumatoid arthritis, convincing evidence is still lacking. Even if an epitope mimic can support a cross-reactive T or B cell response in vitro, its ability to induce an autoimmune disease in vivo will depend upon the appropriate presentation of the mimicked host antigen in the target tissue and, in the case of T cell mimics, the ability of the mimicking epitope to induce a proliferative rather than anergizing response upon engagement of the MHC-peptide complex with the T cell receptor. B cell presentation of mimicking foreign antigen to T cells is a possible mechanism for instigating an autoimmune 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 support of epitope mimicry is examined in the light of the necessary immunological considerations of the theory.

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96 citations in Web of Science®

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ID Code: 87935
Item Type: Journal Article
Refereed: Yes
Keywords: altered peptide ligands, autoimmunity, cross-reactivity, epitope mimicry, molecular mimicry, autoantibody, epitope, HLA antigen class 1, HLA DR2 antigen, HLA DR4 antigen, major histocompatibility antigen class 2, acquired immune deficiency syndrome, ankylosing spondylitis, chagas disease, cross reaction, etiology, guillain barre syndrome, human, insulin dependent diabetes mellitus, nonhuman, pathogenesis, reactive arthritis, review, rheumatic fever, rheumatoid arthritis, Animals, Arthritis, Autoimmune Diseases, B-Lymphocytes, Cross Reactions, Humans, Immune Tolerance, Major Histocompatibility Complex, Models, Immunological, Myocarditis, Parasitic Diseases, Receptors, Antigen, T-Cell
DOI: 10.1038/icb.1997.16
ISSN: 0818-9641
Copyright Owner: Copyright 1997 Nature Publishing Group
Deposited On: 30 Sep 2015 03:02
Last Modified: 30 Sep 2015 03:05

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