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Innate immunity in hypertension topical collection on hypertension and metabolic syndrome

机译:高血压局部代谢对高血压和代谢综合征的先天免疫

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Despite intensive research, the exact cause of hypertension remains unknown. Low-grade inflammation has been proposed to play a key role in the pathogenesis of hypertension. Both innate and adaptive immune responses may participate in this process. Several studies have addressed the contribution of adaptive immunity to the pathophysiology of high blood pressure; however, the role of innate immunity is less clear. Innate immunity may be an important mediator of chronic inflammation in hypertension. Slight elevation of blood pressure due to increased sympathetic and/or decreased parasympathetic outflow, or low-grade infections may generate neoantigens and damage-activated molecular patterns (DAMPs) or pathogen-activated molecular patterns (PAMPs), which can trigger Toll-like receptors on innate effector cells. Innate responses, mediated by monocytes, macrophages, dendritic cells and natural killer cells, may contribute to inflammation either directly or by activating adaptive immune responses mediated by T lymphocytes. In this review, we discuss the recent evidence regarding the contribution of different innate effector cells, their response and their mechanisms of activation in hypertension.
机译:尽管进行了深入的研究,高血压的确切原因仍然未知。已经提出低度炎症在高血压的发病机理中起关键作用。先天和适应性免疫应答都可能参与该过程。多项研究已经论证了适应性免疫对高血压病理生理的贡献。但是,先天免疫的作用尚不清楚。天然免疫可能是高血压慢性炎症的重要介质。由于交感神经增多和/或副交感神经减少导致血压轻微升高,或低度感染可能会产生新抗原和损伤激活分子模式(DAMP)或病原体激活分子模式(PAMP),从而触发Toll样受体在先天效应细胞上。由单核细胞,巨噬细胞,树突状细胞和自然杀伤细胞介导的先天应答可能直接或通过激活由T淋巴细胞介导的适应性免疫应答而导致炎症。在这篇综述中,我们讨论了有关不同先天性效应细胞的贡献,它们的反应及其在高血压中激活机制的最新证据。

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