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Molecular mimicry: a mechanism for autoimmune injury 1
Author(s) -
Barnett Lou Ann,
Fujinami Robert S.
Publication year - 1992
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.6.3.1740233
Subject(s) - molecular mimicry , autoimmunity , mimicry , autoimmune disease , monoclonal antibody , biology , immune system , mechanism (biology) , immunology , antibody , antigen , disease , virus , virology , medicine , ecology , philosophy , epistemology , pathology
Many mechanisms may account for immune‐mediated pathology after viral infections. Although several means have been hypothesized to play a role in disease, a widely accepted mechanism for viral‐induced autoimmunity is molecular mimicry. It is thought that damage could result from an immune response to similar regions shared between virus and the host. Using computer‐aided analysis, many sequence homologies have been identified between virus and host antigens. Using peptides corresponding to these regions, immunologic cross‐reactivity has been found. In some cases, monoclonal antibodies to peptides of these regions have been shown to directly induce or augment disease in animal models. Using this approach to identify similar regions, it is possible to associate a known autoantigen with an infectious agent in autoimmune diseases in which there is no known etiologic agent. Conversely, it would also be possible to associate a known viral constituent with an unknown host antigen. Furthermore, identification of disease‐inducing regions of autoantigens or viral proteins may lead to immunotherapeutic approaches to establish tolerance or anergy to such disease‐inducing regions.—Barnett, L. A. Fujinami, R. S. Molecular mimicry: a mechanism for autoimmune injury. FASEB J. 6: 840‐844; 1992.

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