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.
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.
Impact and interest:
Citation counts are sourced monthly from and citation databases.
These databases contain citations from different subsets of available publications and different time periods and thus the citation count from each is usually different. Some works are not in either database and no count is displayed. Scopus includes citations from articles published in 1996 onwards, and Web of Science® generally from 1980 onwards.
Citations counts from theindexing service can be viewed at the linked Google Scholar™ search.
|Item Type:||Journal Article|
|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|
|Copyright Owner:||Copyright 1997 Nature Publishing Group|
|Deposited On:||30 Sep 2015 03:02|
|Last Modified:||30 Sep 2015 03:05|
Repository Staff Only: item control page