Division of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, North Carolina, USA.
Curr Opin Nephrol Hypertens. 2020 Sep;29(5):515-522. doi: 10.1097/MNH.0000000000000635.
Inflammatory processes play a critical role in the pathogenesis of hypertension. Innate and adaptive immune responses participate in blood pressure (BP) elevation and end-organ damage. In this review, we discuss recent studies illustrating mechanisms through which immune cells and cytokines regulate BP via their actions in the kidney.
Cells of the innate immune system, including monocytes, neutrophils, and dendritic cells, can all promote BP elevation via effects on kidney function. These innate immune cells can directly impact oxidative stress and cytokine generation in the kidney and/or present antigens to lymphocytes for the engagement of the adaptive immune system. Once activated by dendritic cells, effector memory T cells accumulate in the hypertensive kidney and facilitate renal salt and water retention. Individual subsets of activated T cells can secrete tumor necrosis factor-alpha (TNF-α), interleukin-17a (IL-17a), and interferon-gamma (IFN-γ), each of which has augmented the elevation of blood pressure in hypertensive models by enhancing renal sodium transport. B cells, regulate blood pressure via vasopressin receptor 2 (V2R)-dependent effects on fluid transport in the kidney.
Immune cells of the innate and adaptive immune systems drive sodium retention and blood pressure elevation in part by altering renal solute transport.
目的综述：炎症过程在高血压的发病机制中起着关键作用。先天免疫和适应性免疫反应参与血压升高和靶器官损伤。在这篇综述中，我们讨论了最近的研究，这些研究阐明了免疫细胞和细胞因子通过其在肾脏中的作用调节血压的机制。
最新发现：先天免疫系统的细胞，包括单核细胞、中性粒细胞和树突状细胞，都可以通过对肾功能的影响来促进血压升高。这些先天免疫细胞可以直接影响肾脏中的氧化应激和细胞因子生成，或者将抗原呈递给淋巴细胞以激活适应性免疫系统。一旦被树突状细胞激活，效应记忆 T 细胞在高血压肾脏中积累，并促进肾脏盐和水的潴留。活化的 T 细胞的个别亚群可以分泌肿瘤坏死因子-α（TNF-α）、白细胞介素-17a（IL-17a）和干扰素-γ（IFN-γ），它们都通过增强肾脏钠转运来增强高血压模型中血压的升高。B 细胞通过对肾脏中液体转运的血管加压素受体 2（V2R）依赖性作用来调节血压。
总结：先天和适应性免疫系统的免疫细胞通过改变肾脏溶质转运来驱动钠潴留和血压升高。
