Immunopathogenesis of atherosclerosis

Journal of Leukocyte Biology

Burkhard Ludewig¹  Elke Scandella¹  Philippe Krebs¹ 

[1] Research Department, Kantonal Hospital St. Gallen, SwitzerlandResearch Department, Kantonal Hospital St. Gallen, SwitzerlandResearch Department, Kantonal Hospital St. Gallen, Switzerland

关键词: immunopathology;    bystander activation;    molecular mimicry;    transgenic mouse model;   

DOI  :  10.1189/jlb.1203605

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

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.

【 授权许可】

Unknown