Kawasaki disease and stress protein.
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概要
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Kawasaki disease, an acute febrile illness which affects infants and young children, is characterized by diffuse mucosal inflammation, indurative edema, polymorphous rash, and nonsuppurative cervical lymphadenopathy. About 15-20% of patients suffer coronary arterial damage, and they may develop myocardial infarction, chronic coronary insufficiency, and sudden death. Since Kawasaki originally described this disease entity in 1967, the number of such patients in Japan has reached 100, 000.<BR>While the etiology is still unknown, the epidemiological features of this disease indicate that it is related to an infectious agent. Immunologically, both a highly increased level of several cytokines and the activation of immunocompetent cells have been demonstrated. Pathology have revealed that the vascular lesion begins with endothelial cell damage, the initial step of which may be activation of the endothelial cell to express ICAM-1 and ELAM-1 by cytokines. Thus, the etiologic factor (s) would predispose to an activation of both the immune system and the endothelial cells.<BR>Some mitogenic materials including superantigen, stress protein, and so forth, would be the candidates. According to the clinical findings, inflammatory changes at the site of a previous BCG inoculation seems to be an early and specific manifestation of Kawasaki diseasse. We postulated that molecule (s) that are cross-reactive between the suspected infectious agent and the mycobacterial BCG antigen may contribute to this inflammatory process. Using BCG lysates or recombinant stress protein, HSP65, as antigen for Western blotting, convalescent, but not acute, phase sera of Kawasaki disease did react with HSP65 antigen, suggesting bacterial stress protein may be the causative agent which abnormally activate immune system. Moreover, epitope mapping of human mitochondrial protein, P1 antigen, indicated that convalescent phase sera of Kawasaki disease contained autoantibody to this human HSP65 cognate antigen.<BR>Thus, Kawasaki disease may be induced by the exposure of bacterial HSP65, and recognition of autologous HSP65 cognate antigen by activated immune system may exaggerate the autoimmune response.
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