期刊
ANNUAL REVIEW OF IMMUNOLOGY
卷 22, 期 -, 页码 361-403出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.immunol.22.012703.104644
关键词
aging; inflammation; heat shock proteins; infections; signal transduction
类别
The present review focuses on the concept that cellular and humoral immunity to the phylogenetically highly conserved antigen heat shock protein 60 (HSP60) is the initiating mechanism in the earliest stages of atherosclerosis. Subjecting arterial endothelial cells to classical atherosclerosis risk factors leads to the expression of HSP60 that then may serve as a target for pre-existent cross-reactive antimicrobial HSP60 immunity or bona fide autoimmune reactions induced by biochemically altered autologous HSP60. Endothelial cells can also bind microbial or autologous HSP60 via Toll-like receptors, providing another possibility for targetting adaptive or innate immunological effector mechanisms.
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