Autoantibody against beta(1)-adrenoceptor (beta(1)-AA) has been shown to be closely linked to the aggravation of heart failure. Removal of beta(1)-AA remarkably attenuated patients' cardiac dysfunction. We found that beta(1)-AA induced rat heart failure with increased CD4(+) T cells. However, whether or not beta(1)-AA interacts with T cells isolated from heart failure patients remains unknown. Twenty-one beta(1)-AA-negative heart failure patients were divided into those taking beta-adrenergic blocker and those not. The effects of beta(1)-AA monoclonal antibodies (beta(1)-AAmAb) on T cells proliferation were detected using the CCK-8 assay. IFN-gamma and IL-4 production by human T cells were measured by after the administration of beta 1-AAmAb. The levels of cardiomyocyte apoptosis and hypertrophy were detected after co-cultured with the supernatant of T cells pre-stimulated by beta(1)-AAmAb. It was found that beta(1)-AAmAb promoted T cell proliferation via the beta 1-AR/cAMP/PKA pathway in patients who not take beta-blocker. beta(1)-AAmAb inhibited the characteristic cytokine secretion of Th1, IFN-gamma, but had no significant effect on the Th2 cytokine IL-4. Supernatant resulted from the T cells pre-treated with beta(1)-AAmAb induced cardiomyocytes remodeling, as evidenced by increased levels of cardiomyocytes apoptosis and hypertrophy. We propose that heart failure is likely to be an interference factor for Th-mediated immunity, and the presence of beta(1)-AAmAb may aggravate this effect and deteriorate concomitant inflammatory injury in cardiomyocytes, partially via beta(1)-AR/cAMP/PKA pathway. (C) 2019 Elsevier Inc. All rights reserved.