Activation of T Lymphocytes as a Novel Mechanism in Beta1-Adrenergic Receptor Autoantibody-Induced Cardiac Remodeling

Diagnostic and prognostic value of autoantibodies against β1‑adrenoreceptors in patients with heart failure following acute myocardial infarction: A 5‑year prospective study

“…In addition, it was observed that β 1 R-AAbs, similar to isoproterenol receptor agonists, activate protein kinase A to phosphorylate several phosphoproteins in the cells (33). Prolonged overstimulation of β 1 -ARs may lead to deterioration in heart function and the underlying mechanism is considered to be the induction of apoptosis by T-lymphocytes (34). β 1 R-AAbs exerted pro-apoptotic effects with increased generation of phenyl glycidyl ether.…”

Activation of T Lymphocytes as a Novel Mechanism in Beta1-Adrenergic Receptor Autoantibody-Induced Cardiac Remodeling—Additional Information About TLR9 Involvement

“…These authors observed that, besides the already welldescribed activation of the beta1-adrenoceptors directly in the heart cells [2,3], these autoantibodies additionally activated beta1-adrenoceptors in T lymphocytes [1]. Via the latter, the autoantibodies caused IL-6 release which is, according to their results, a further contributing factor to the pathogenesis of heart failure.…”

“…Both studies together complete a general understanding of the effects of TLR9 on the initiation and subsequent mainte-nance of heart failure that creates a vicious circle by making TLR9 essential in autoantibody formation [4], which in turn, stimulate receptors in heart cells and T lymphocytes [1].…”

“…Du et al [1] with their recently published interesting investigations on T cell activation caused by beta1-adrenoceptor autoantibodies represent another piece of the puzzle in identifying the entire pathological way of action of these agonistic acting autoantibodies in the pathogenesis of heart disease.…”

Role of autoantibodies against cardiomyocyte antigens in the development of cardiac arrhythmiae and sudden cardiac death

“…Имеются сведения, что митохондриальная ДНК при нарушении аутофагии может инициировать воспалительный процесс через активацию Toll-подобного рецептора 9-го типа (TLR9) с развитием миокардита/дилатационной КМП [54]. Анти-β1-AР ауто-АТ также способы стимулировать пролиферацию Т-лимфоцитов человека и продукцию ими провоспалительного цитокина IL-6 через активацию β1-AР на лимфоцитах [55]. При добавлении к культуре кардиомиоцитов надосадочной жидкости, полученной при центрифугировании Т-лимфоцитов, предварительно обработанных анти-β1-AР ауто-АТ, наблюдалось усиление процессов апоптоза и гипертрофии в культуре клеток [56].…”