Immuno-inflammatory processes are implicated, as one of the prime pathogenic processes involved, in the development and progression of early atherosclerosis. High levels of circulating antiheat shock protein 60 (HSP60) autoantibodies have been associated with increasing severity of atherosclerosis in patients. We have recently presented evidence, extending this statistical association to that of causality, by showing that anti-HSP60 antibodies purified from sera of patients with documented atherosclerosis when injected into tail vein of apoE deficient mice resulted in accelerated atherosclerosis in them. High degree of sequence homology between microbial and mammalian HSP60, due to evolutionary conservation, carries a risk of misdirected autoimmunity against HSPs expressed on the stressed cells of vascular endothelium. HSPs and anti-HSP antibodies have been shown to elicit production of pro-inflammatory cytokines. These autoimmune reactions to HSPs expressed in the vascular tissue can contribute to both initiation and perpetuation of atherosclerosis.
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