High blood pressure is present in more than one billion adults worldwide and is the most important modifiable risk factor of death resulting from cardiovascular disease. While many factors contribute to the pathogenesis of hypertension, a role of the immune system has been firmly established by a large number of investigations from many laboratories around the world. Immunosuppressive drugs and inhibition of individual cytokines prevent or ameliorate experimental hypertension, and studies in genetically-modified mouse strains have demonstrated that lymphocytes are necessary participants in the development of hypertension and in hypertensive organ injury. Furthermore, immune reactivity may be the driving force of hypertension in autoimmune diseases. Infiltration of immune cells, oxidative stress, and stimulation of the intrarenal angiotensin system are induced by activation of the innate and adaptive immunity. High blood pressure results from the combined effects of inflammation-induced impairment in the pressure natriuresis relationship, dysfunctional vascular relaxation, and overactivity of the sympathetic nervous system. Imbalances between proinflammatory effector responses and anti-inflammatory responses of regulatory T cells to a large extent determine the severity of inflammation. Experimental and human studies have uncovered autoantigens (isoketal-modified proteins and heat shock protein 70) of potential clinical relevance. Further investigations on the immune reactivity in hypertension may result in the identification of new strategies for the treatment of the disease.

中文翻译：

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免疫系统在高血压中的作用。


全球有超过十亿成年人患有高血压，是心血管疾病导致死亡的最重要的可改变危险因素。虽然许多因素导致高血压的发病机制，但世界各地许多实验室的大量研究已明确证实免疫系统的作用。免疫抑制药物和抑制个体细胞因子可预防或改善实验性高血压，对转基因小鼠品系的研究表明，淋巴细胞是高血压发展和高血压器官损伤的必要参与者。此外，免疫反应可能是自身免疫性疾病中高血压的驱动力。先天免疫和适应性免疫的激活可诱导免疫细胞的浸润、氧化应激和肾内血管紧张素系统的刺激。高血压是由炎症引起的压力尿钠关系受损、血管舒张功能失调和交感神经系统过度活跃的综合影响造成的。调节性T细胞的促炎效应反应和抗炎反应之间的不平衡在很大程度上决定了炎症的严重程度。实验和人体研究发现了具有潜在临床意义的自身抗原（异缩酮修饰蛋白和热休克蛋白 70）。对高血压免疫反应性的进一步研究可能会导致确定治疗该疾病的新策略。