Regulation of T Cell Level and Composition by Angiotensin II and Estrogens in Arterial Hypertension

Abstract Arterial hypertension is characterized by the development of chronic indolent inflammation, activation of innate and adaptive immunity cells. The number and activity of certain subsets of T cells changes. This is probably the key mechanism for the development and maintenance of chronic inflammation in this disease. Hormones such as angiotensin II (Ang II), estrogens and testosterone affect the profile and characteristics of T cells. High levels of angiotensin II contribute to a decrease in the number of Foxp3+ cells, an increase in the number of monocytes, Th1, Th2 and Th17. Age and gender differences in the number of T cells are shown. With age the number of naive T cells decreases, senescent lymphocytes increase, T cell activity and production of proinflammatory cytokines increase. These changes in the T cell balance probably contribute to the creation of a proinflammatory environment in the body and an increased risk of developing high blood pressure. The number of T cells and their functional activity depend on the level of estrogens. This affects the incidence and severity of hypertension in postmenopausal women. Modulation of estrogen levels and estrogen receptor activity may serve as promising approaches to prevent the development of arterial hypertension.