Dragun Duska, Philippe Aurélie, Catar Rusan, Hegner Björn
Department of Nephrology and Intensive Care Medicine, Charité Campus Virchow Clinic, Berlin, Germany.
Thromb Haemost. 2009 Apr;101(4):643-8.
Antibodies directed against G-protein coupled receptors (GPCR) can act as allosteric receptor agonists or antagonists. Prototypic disease for agonistic antibody action is a Graves disease of the thyroid gland where antibodies that stimulate G-protein coupled thyroid-stimulating hormone receptor (TSHR) were first described 50 years ago. Myasthenia gravis is the prototype for antagonistic autoimmune actions, where antibodies directed against the nicotinic acetylcholine receptor (AChR) cause blockade of neuromuscular junctions. Antibodies and B-cells are increasingly recognised as major modulators of various cardiovascular and renal pathologies. We aim to critically review the notion that antibodies targeting other GPCRs may amplify or cause various cardiovascular and renal pathologies and summarise the current state of research, as well as perspectives in diagnostic and therapeutic strategies. In terms of targets we will focus on the alpha-adrenergic receptor (alpha(1)AR), the beta-adrenergic receptor (beta(1)AR), and the angiotensin II type 1 receptor (AT(1)R).
针对G蛋白偶联受体（GPCR）的抗体可作为变构受体激动剂或拮抗剂。激动性抗体作用的典型疾病是甲状腺的格雷夫斯病，50年前首次描述了刺激G蛋白偶联促甲状腺激素受体（TSHR）的抗体。重症肌无力是拮抗性自身免疫作用的典型例子，其中针对烟碱型乙酰胆碱受体（AChR）的抗体导致神经肌肉接头的阻断。抗体和B细胞越来越被认为是各种心血管和肾脏疾病的主要调节因子。我们旨在批判性地审视靶向其他GPCR的抗体可能会放大或导致各种心血管和肾脏疾病这一观点，并总结当前的研究状况以及诊断和治疗策略的前景。在靶点方面，我们将重点关注α-肾上腺素能受体（α(1)AR）、β-肾上腺素能受体（β(1)AR）和血管紧张素II 1型受体（AT(1)R）。
