Abstract

Clinical and pathological manifestations present as heterogeneous in vasculitides. Thus, inflammation can affect arteries, arterioles, capillaries, venules, and veins toward major body regions. One common feature of vascular diseases appears to be the presence of anti-HSP60 autoantibodies arising either consecutively to infection and molecular mimicry reaction with bacterial HSP60, or following recognition of endogenous HSP60 translocated or bound onto the surface of stressed endothelial cells. Because their levels are very low in some diseases but strikingly upregulated in others, and because their frequencies vary from one vasculitis to another, anti-HSP60 autoantibodies might play a role in the pathological mechanisms that likely differ among the vascular diseases. Identification of the variety of HSP60 epitope specificities along with each vasculitis would help to understand such discrepancies.

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