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Infection as a Precursor to Autoimmunity

  • Noel R. Rose
Part of the Infectious Agents and Pathogenesis book series (IAPA)

Abstract

The ability to distinguish self from nonself is a cardinal feature of the normal immune system. Nevertheless, the development of autoimmune responses is a common occurrence. Many mechanisms have been proposed to explain the failure of self/nonself discrimination. Of the explanations offered, the intervention of infection is among the most conspicuous. Indeed, the first example of an autoimmune disease, paroxysmal cold hemoglobinuria, was originally attributed to syphilitic infection.1 In the recent literature, insulin-dependent diabetes mellitus has been associated with Coxsackievirus Group B infection.2 Despite intensive research in many laboratories, however, scanty information is available on the mechanisms by which infection may function to precipitate autoimmune disease. Some investigators have cited examples of molecular mimicry, based on homology between an amino acid sequence of some endogenous antigen and an antigen of a pathogen.3 Other investigations pointed to an effect of infection on the regulation of the immune response.4 Still others have suggested that an infectious agent may produce changes in self-antigens.5 None of these mechanisms, however, has yet been proven to cause an actual autoimmune disease.

Keywords

Molecular Mimicry Cardiac Myosin Adenine Nucleotide Translocator Autoimmune Myocarditis Skeletal Myosin 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1996

Authors and Affiliations

  • Noel R. Rose
    • 1
  1. 1.Departments of Pathology and of Molecular Microbiology and ImmunologyThe Johns Hopkins Medical InstitutionsBaltimoreUSA

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