T-CELL RESPONSES TO CONSERVED BACTERIAL HEAT-SHOCK-PROTEIN EPITOPES INDUCE RESISTANCE IN EXPERIMENTAL AUTOIMMUNITY

The relationships between bacterial heat shock proteins (HSPs) and aut oimmunity were first disclosed in the mycobacteria-induced model of ad juvant arthritis: passive trans fer of a T cell clone responding to my cobacterial HSP60 evoked disease in naive recipient animals. However, the disease could not be induced by immunization with HSP60, but inste ad protection was established. Subsequently, similar protection was fo und in experimental models of arthritis that do not involve challenge with bacterial antigens for the induction, of disease. This rather gen eral protective potency of bacterial HSPs against arthritis seems to r esult from the capacity of strongly conserved sequences in the protein to activate T cells that moss-recognize the mammalian homologous HSP- sequences presented on cells at the site of inr flammation. It is poss ible that immunological recognition of bacterial HSPs is part of a gen eral strategy used by the immune system for the regulatory control of the potentially harmful recognition of autoantigens as a hedge against the development of autoimmune disease.