Dysregulation of T cell subsets in the pathogenesis of hypertension.

Dysregulation of T cell subsets in the pathogenesis of hypertension.
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DOI:
10.1007/s11906-014-0521-1
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发表时间:
2015-03
影响因子:
5.6
通讯作者:
Agrawal DK
Agrawal DK
中科院分区:
医学2区
文献类型:
--
作者:
Chen S;Agrawal DK

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原发性高血压(EH)及其并发症已严重影响公众健康。然而,高血压的发病机制仍不清楚。最近的研究,主要是在大鼠和小鼠,提供了证据表明,T淋巴细胞亚群的不同功能的失调是一个潜在的重要机制,在高血压的发病机制。我们批判性地回顾了最近的研究结果,并提出了另一种解释的理解功能失调的T淋巴细胞亚群在高血压的发病机制。假设高血压刺激,直接和间接,增加局部IL-6水平在心血管系统和肾脏,这可能会促进外周失衡的分化和比例的Th 17和T调节细胞。这导致在实验动物模型中血管周围脂肪组织和外膜中IL-17增加和IL-10减少,从而促进高血压的发展。因此,有必要对该领域进行深入研究,以了解新的转化进展,从而促进对EH发病机制的了解,并开发新的预防和治疗EH的方法。
Essential hypertension (EH) and its complications have had a severe impact on public health. However, the underlying mechanisms of the pathogenesis of EH remain largely unknown. Recent investigations, predominantly in rats and mice, have provided evidence that dysregulation of distinct functions of T lymphocyte subsets is a potentially important mechanism in the pathogenesis of hypertension. We critically reviewed recent findings and propose an alternative explanation on the understanding of dysfunctional T lymphocyte subsets in the pathogenesis of hypertension. The hypothesis is that hypertensive stimuli, directly and indirectly, increase local IL-6 levels in the cardiovascular system and kidney, which may promote peripheral imbalance in the differentiation and ratio of Th17 and T regulatory cells. This results in increased IL-17 and decreased IL-10 in perivascular adipose tissue and adventitia contributing to the development of hypertension in experimental animal models. Further investigation in the field is warranted to inform new translational advances that will promote to understand the pathogenesis of EH and develop novel approaches to prevent and treat EH.
适应性免疫系统在高血压中的作用。
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