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Published online before print March 23, 2004
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1203605

Received for publication December 1, 2003.
Revised February 12, 2004.
Accepted for publication February 16, 2004.

Article

Immunopathogenesis of atherosclerosis

Burkhard Ludewig @, Philippe Krebs , and Elke Scandella

Research Department, Kantonal Hospital St. Gallen, Switzerland

@ To whom correspondence should be addressed. E-mail: Burkhard.Ludewig{at}kssg.ch.


  Abstract

Recent clinical studies indicate that the number of microbial infections (the "pathogen burden") critically determines the development and progression of atherosclerotic disease. Viruses or bacteria with a specific tropism for cells of the vascular wall may contribute to the initial vascular injury via direct cytopathic effects or via the induction of genuine autoimmune responses. Immunopathological processes such as molecular mimicry, epitope spreading, or bystander activation of self-reactive lymphocytes most likely fuel the chronic inflammatory process in the vascular wall. Recognition of atherogenesis as a pathogen-driven, immunopathological process makes this disease amenable to new treatment strategies such as vaccination or immunomodulation.

Key Words: immunopathology • bystander activation • molecular mimicry • transgenic mouse model




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