Title: Molecular mimicry and immune‐mediated diseases
Abstract: The FASEB JournalVolume 12, Issue 13 p. 1255-1265 ReviewFree to Read Molecular mimicry and immune-mediated diseases Michael B. A. Oldstone, Corresponding Author Michael B. A. Oldstone [email protected] Viral Immunobiology Laboratory, Division of Virology, The Scripps Research Institute, Department of Neuropharmacology, La Jolla, California, 92037 USA Correspondence: Viral Immunobiology Laboratory, Division of Virology, The Scripps Research Institute, Department of Neuropharmacology, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA. E-mail: [email protected]Search for more papers by this author Michael B. A. Oldstone, Corresponding Author Michael B. A. Oldstone [email protected] Viral Immunobiology Laboratory, Division of Virology, The Scripps Research Institute, Department of Neuropharmacology, La Jolla, California, 92037 USA Correspondence: Viral Immunobiology Laboratory, Division of Virology, The Scripps Research Institute, Department of Neuropharmacology, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA. E-mail: [email protected]Search for more papers by this author First published: 01 October 1998 https://doi.org/10.1096/fasebj.12.13.1255Citations: 408Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Molecular mimicry has been proposed as a pathogenetic mechanism for autoimmune disease, as well as a probe useful in uncovering its etiologic agents. The hypothesis is based in part on the abundant epidemiological, clinical, and experimental evidence of an association of infectious agents with autoimmune disease and observed cross-reactivity of immune reagents with host ‘self’ antigens and microbial determinants. For our purpose, molecular mimicry is defined as similar structures shared by molecules from dissimilar genes or by their protein products. Either the molecules' linear amino acid sequences or their conformational fits may be shared, even though their origins are as separate as, for example, a virus and a normal host–self determinant. An immune response against the determinant shared by the host and virus can evoke a tissue-specific immune response that is presumably capable of eliciting cell and tissue destruction. The probable mechanism is generation of cytotoxic cross-reactive effector lymphocytes or antibodies that recognize specific determinants on target cells. The induction of cross-reactivity does not require a replicating agent, and immune-mediated injury can occur after the immunogen has been removed—a hit-and-run event. Hence, the viral or microbial infection that initiates the autoimmune phenomenon may not be present by the time overt disease develops. By a complementary mechanism, the microbe can induce cellular injury and release self antigens, which generate immune responses that cross-react with additional but genetically distinct self antigens. In both scenarios, analysis of the T cells or antibodies specifically engaged in the autoimmune response and disease provides a fingerprint for uncovering the initiating infectious agent.—Oldstone, M. B. A. Molecular mimicry and immune-mediated diseases. FASEB J. 12, 1255–1265 (1998) REFERENCES 1Theofilopoulos, A. (1995) The basis of autoimmunity. II. Genetic predisposition. Immunol. Today 16, 150–159 10.1016/0167-5699(95)80133-2 CASPubMedWeb of Science®Google Scholar 2Merriman, T. 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