Sex differences in blood pressure control: are T lymphocytes the missing link?
Sex differences in blood pressure control: are T lymphocytes the missing link?
复制标题
血压控制的性别差异：T 淋巴细胞是缺失的一环吗？
DOI：
10.1161/hypertensionaha.114.03688
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Sullivan,JenniferC
中科院分区：
文献类型：
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作者：
Tipton,AshleeJ;Sullivan,JenniferC
DOI: 10.1161/HYPERTENSIONAHA. 114.03688 necrosis factor-α after Ang-II infusion that were not found in the female, suggesting an increase in the overall inflammatory profile only in the male. Regardless, the authors clearly demonstrate that female Rag−/− mice limit the prohypertensive effects of T lymphocytes from males in Ang-II hypertension. Understanding the mechanisms by which females achieve this relative cardioprotection could provide important insight into novel mechanisms to regulate BP in both sexes. Although it has been established that T lymphocytes play a significant role in the development of hypertension, the effect of different T-lymphocyte subtypes on BP control remains debatable in males and unexplored in females. It should be noted that although the study by Pollow et al3 did not find an increase in renal T lymphocytes in either sex after Ang-II infusion, T-lymphocyte activation was not assessed and neither were proinflammatory, prohypertensive T helper 17 (Th17) cells. 3 Th17 cells are effector T lymphocytes that exert their effector function by the secretion of interleukin-17, interleukin-21, and interleukin-23. Interestingly, male interleukin-17 knockout mice have an attenuated increase in BP after Ang-II infusion, implicating Th17 cells in Ang-II–induced increases in BP. 4 In line with this observation, we have previously shown that male spontaneously hypertensive rats (SHR) have greater renal Th17 cell infiltration and higher BP than female SHR, and hypertension in SHR is sensitive to Ang-II inhibition. Based on these data, it would have been interesting to know how sex and Ang-II affected Th17 cells in Rag−/− mice. In contrast, Tregs are anti-inflammatory T lymphocytes that suppress immune effector function through the secretion of interleukin-10 and female SHR have more Tregs in their kidneys than males. Direct support for Tregs to modulate BP comes from studies where adoptive transfer of Tregs attenuates Ang-II–induced increases in BP in male mice. 5 Because these T-lymphocyte subsets potentially have opposing effects on BP regulation, defining T-lymphocyte subtypes and examining the ratio of Th17 cells to Tregs may be critical to understanding the role of T lymphocytes in BP control in both sexes. Moreover, because studies suggest differential roles for these T-lymphocyte subtypes on BP, it is not unreasonable to postulate that the sex difference in the balance of Th17 cells and Tregs may contribute to observed sex differences in BP control.It is attractive to hypothesize that the current study by Pollow et al3 and the immune system may hold the key for tying together the extensive literature documenting sex differences in cardiovascular disease. There are numerous reports of sex differences in BP and cardiovascular disease both in genetic models of hypertension and in Ang-II–induced hypertension.
