This review highlights the potential shared pathophysiological mechanisms involving anti-beta(1)-adrenoceptor autoantibodies in Chagas' heart disease and idiopathic dilated cardiomyopathy.
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Does not change cardiomyopathy management; hypothesis-generating for shared autoimmunity across Chagas' and idiopathic forms.
Anti-beta(1)-adrenoceptor autoantibodies, first described in sera of patients with Chagas' disease, are now well documented in patients with idiopathic dilated cardiomyopathy. The following review summarizes the knowledge we have about the structural basis of receptor-antibody interactions, about their mechanisms of action and about their pathogenicity. While the origin of anti-receptor antibodies with agonist-like activity in Chagas' disease might be ascribed to recognition by anti-parasite antibodies of an epitope, localized on the second extracellular loop of the beta(1)-adrenoceptor, the origin of such antibodies in idiopathic dilated cardiomyopathy remains unknown. The hypothesis of a similar origin for anti-receptor antibodies in both diseases is forwarded.
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Levin et al. (2008) studied this question.
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