Heartache of fc receptors.

diopathic dilated cardiomypathy (DCM) is characterized y the progressive depression of cardiac function and left entricular dilation in the absence of coronary artery disease. here is evidence to suggest that humoral immunity plays n important role in the pathogenesis of DCM. In particlar, the role of autoantibodies in the pathogenesis of DCM as been emphasized (1). Sera from patients with DCM how a variety of autoantibodies, including those against embrane proteins, mitochondrial proteins, heat-shock roteins, and myocyte structural sarcolemmal proteins. Beause all these antibodies are not present in each patient ith DCM, it is apparent that all these autoantibodies are ot pathogenic in DCM. To date, only 2 autoantibodies ave satisfied the criteria of cause-and-effect relationship for CM, and both these antibodies display stimulatory activties. The first comes from a report that program death eceptor-1 (PD-1) mice develop autoantibodies against ardiac troponin 1 (cTpn 1) and dilated heart, and second rom the finding that the injection of autoantibodies against Tpn-1 from these mice into normal mice induces dilation nd dysfunction of the heart in recipient mice (2), therefore stablishing a direct role of anti–cTpn-1 antibody in dilaion and dysfunction of heart resembling human DCM.