Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation also plays an important role in the pathophysiology and contributes to the deleterious consequences of this disease. Cells of the innate immune system including monocyte/macrophages and dendritic cells can promote blood pressure elevation via effects mostly on kidney and vascular function. Moreover, convincing evidence shows that T and B cells from the adaptive immune system are involved in hypertension and hypertensive end-organ damage. Skin monocyte/macrophages, regulatory T cells, natural killer T cells, and myeloid-derived suppressor cells have been shown to exert blood pressure controlling effects. Sodium intake is undoubtedly indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake. Modulation of the immune response can reduce severity of blood pressure elevation and hypertensive end-organ damage in several animal models. The purpose of this review is to briefly summarize recent advances in immunity and hypertension as well as hypertensive end-organ damage.

中文翻译：

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动脉高血压的免疫机制。近期进展

越来越多的证据表明，高血压和高血压终末器官损伤不仅由血流动力学损伤介导。炎症在病理生理学中也起着重要作用，并导致这种疾病的有害后果。包括单核细胞/巨噬细胞和树突状细胞在内的先天免疫系统细胞可以通过主要影响肾脏和血管功能来促进血压升高。此外，令人信服的证据表明，适应性免疫系统中的 T 细胞和 B 细胞与高血压和高血压终末器官损伤有关。皮肤单核细胞/巨噬细胞、调节性 T 细胞、自然杀伤 T 细胞和髓源性抑制细胞已被证明具有控制血压的作用。钠的摄入量对于正常的身体机能来说无疑是必不可少的，但如果摄入量超过饮食要求则可能是有害的。钠水平还调节单核细胞/巨噬细胞、树突细胞和不同 T 细胞亚群的功能。其中一些影响是由高盐摄入后微生物组和代谢组的变化介导的。在几种动物模型中，免疫反应的调节可以降低血压升高和高血压终末器官损伤的严重程度。本综述的目的是简要总结免疫和高血压以及高血压终末器官损害方面的最新进展。其中一些影响是由高盐摄入后微生物组和代谢组的变化介导的。在几种动物模型中，免疫反应的调节可以降低血压升高和高血压终末器官损伤的严重程度。本综述的目的是简要总结免疫和高血压以及高血压终末器官损害方面的最新进展。其中一些影响是由高盐摄入后微生物组和代谢组的变化介导的。在几种动物模型中，免疫反应的调节可以降低血压升高和高血压终末器官损伤的严重程度。本综述的目的是简要总结免疫和高血压以及高血压终末器官损害方面的最新进展。