Modulation of endothelial cell damages by anti-Hsp60 autoantibodies in systemic autoimmune diseases.

Heat-shock protein (Hsp) family is made up of heterogeneous proteins of which Hsp60 members are the most studied. It is now generally admitted that Hsp60 is not only a mitochondrial component but can be localized on the membrane cell surface. Considered as a signal danger following infections, Hsp60 can induce the production of anti-Hsp60 antibodies as defense mechanisms against pathogens. However, endogenous Hsp60 is also a target of autoantibodies in autoimmune disorders, atherosclerosis and vascular diseases, in which anti-endothelial cell antibodies (AECA) are generated. Hsp60 is one of the endothelial cell autoantigens able to trigger cytotoxic and apoptotic responses when recognized by the related autoantibodies. Depending on the Hsp60 epitope specificity, it appears that AECA with Hsp60 reactivity may differ in their functional effects. These observations suggest that new therapeutic approach to avoid endothelial cell damages due to anti-Hsp60 autoantibodies would be successful provided that specific Hsp60 epitopes would have been precisely characterized.