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Previous Volume 341:2068-2074 December 30, 1999 Number 27 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Autoimmune disease is the consequence of an immune response against self-antigens that results in the damage and eventual dysfunction of target organs. Although the triggering event in most autoimmune diseases is unknown, an infectious cause has long been postulated to explain the development of autoimmunity. Molecular mimicry is one mechanism by which infectious agents (or other exogenous substances) may trigger an immune response against autoantigens. According to this hypothesis a susceptible host acquires an infection with an agent that has antigens that are immunologically similar to the host antigens but differ sufficiently to induce an immune response when presented to . . . [Full Text of this Article]

The Immunologic Basis of Molecular Mimicry

Sequence or Structural Homology

Key Issues in Molecular Mimicry

Experimental Models

Clinical Candidates for Molecular Mimicry

Conclusions

Source Information

From the Division of Rheumatology, Department of Medicine, Toronto Western Hospital, University Health Network (L.J.A., R.D.I.); and the Departments of Medicine (L.J.A., R.D.I.) and Immunology (R.D.I.), University of Toronto — both in Toronto.

Address reprint requests to Dr. Inman at the Arthritis Center of Excellence, Toronto Western Hospital, FP 1-221, 399 Bathurst St., Toronto, ON M5T 2S8, Canada, or at rinman@torhosp.toronto.on.ca.

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