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先天性和适应性免疫系统会引发高血压吗?

Are the innate and adaptive immune systems setting hypertension on fire?

作者信息

Bomfim Gisele F, Rodrigues Fernanda Luciano, Carneiro Fernando S

机构信息

Institute of Health Sciences, Federal University of Mato Grosso, Sinop, MT, Brazil.

Department of Physiology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, SP, Brazil.

出版信息

Pharmacol Res. 2017 Mar;117:377-393. doi: 10.1016/j.phrs.2017.01.010. Epub 2017 Jan 16.

DOI:10.1016/j.phrs.2017.01.010
PMID:28093357
Abstract

Hypertension is the most common chronic cardiovascular disease and is associated with several pathological states, being an important cause of morbidity and mortality around the world. Low-grade inflammation plays a key role in hypertension and the innate and adaptive immune systems seem to contribute to hypertension development and maintenance. Hypertension is associated with vascular inflammation, increased vascular cytokines levels and infiltration of immune cells in the vasculature, kidneys and heart. However, the mechanisms that trigger inflammation and immune system activation in hypertension are completely unknown. Cells from the innate immune system express pattern recognition receptors (PRR), which detect conserved pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) that induce innate effector mechanisms to produce endogenous signals, such as inflammatory cytokines and chemokines, to alert the host about danger. Additionally, antigen-presenting cells (APC) act as sentinels that are activated by PAMPs and DAMPs to sense the presence of the antigen/neoantigen, which ensues the adaptive immune system activation. In this context, different lymphocyte types are activated and contribute to inflammation and end-organ damage in hypertension. This review will focus on experimental and clinical evidence demonstrating the contribution of the innate and adaptive immune systems to the development of hypertension.

摘要

高血压是最常见的慢性心血管疾病,与多种病理状态相关,是全球发病和死亡的重要原因。低度炎症在高血压中起关键作用,先天性和适应性免疫系统似乎促进了高血压的发生和维持。高血压与血管炎症、血管细胞因子水平升高以及免疫细胞浸润血管、肾脏和心脏有关。然而,高血压中引发炎症和免疫系统激活的机制完全未知。先天性免疫系统的细胞表达模式识别受体(PRR),其检测保守的病原体相关分子模式(PAMP)和损伤相关分子模式(DAMP),这些模式诱导先天性效应机制产生内源性信号,如炎性细胞因子和趋化因子,以提醒宿主存在危险。此外,抗原呈递细胞(APC)作为哨兵,被PAMP和DAMP激活以感知抗原/新抗原的存在,继而激活适应性免疫系统。在这种情况下,不同类型的淋巴细胞被激活,并导致高血压中的炎症和终末器官损伤。本综述将聚焦于实验和临床证据,以证明先天性和适应性免疫系统对高血压发展的作用。

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