Hypertension is a cardiovascular syndrome with elevated blood pressure as the main clinical manifestation, with or without multiple cardiovascular risk factors, and is the most important cause and risk factor for many cardiovascular and cerebrovascular diseases. Current studies have found that the pathogenesis of hypertension mainly includes the following aspects: neural mechanism, renal mechanism, hormonal mechanism, vascular mechanism, and insulin resistance [1].In 1970, Ebringer and Doyle [2] found that 30% of patients with hypertension were accompanied by a significant increase in serum immunoglobulin levels. In recent years, a large number of studies have shown that hypertension is often accompanied by abnormal immune function and that immune factors are involved in the development and progression of hypertensive complications. The purpose of this article is to provide a brief review of the relationship between hypertension and regulatory T cells. 1, T lymphocyte subpopulation According to the different functions in the immune response, T cells can be divided into several subpopulations: cytotoxic T cells, with the function of killing target cells, the main surface marker is CD8, also known as killer T cells; helper T cells play the role of intermediate process in the immune response: it can proliferate and spread to activate other types of immune cells that produce direct immune response, the main surface marker is CD4; regulatory/suppressor T cells are responsible for regulating the body’s immune response and usually play a role in maintaining self-tolerance and avoiding an excessive immune response. There are many types of regulatory/suppressor T cells the most studied are CD4+CD25+ T cells; effector T cells, which have the function of releasing lymphokines; memory T cells (Tm), which have the role of remembering specific antigenic stimuli; delayed metaplastic T cells (Td), which have the role of participating in type IV metaplastic reactions; amplifying T cells (Ta), which can act on Th and Ts and have an expanded immune effect role; natural T cells, they differentiate into effector T cells and memory T cells after contact with antigen. 2, regulatory T cells 2, 1 Classification of regulatory T cells Regulatory T cells can be divided into naturally occurring natural regulatory T cells (nTreg), mainly CD4+CD25+ Treg; induced adaptive regulatory T cells (aTreg or iTreg), which develop from peripheral naïve T cells induced by small doses of antigen or immunosuppressive cytokines. It includes Tr1, Th3 and other cells, which mainly secrete IL-10 and TGF-β to play a negative immune regulatory role; CD+8 regulatory T cells, which are mainly derived from CD+8 CD-28 T lymphocytes in human; natural killer T cells (NKT), which are a unique group of αβ T cells that express T cell receptor TCRαβ, in addition to NK cell receptor NK1.1 or NK161. 2,2 Physiological characteristics of regulatory T cells Regulatory T cells (Treg) are a subpopulation of T cells with two major functions: immune incompetence and immunosuppression, of which the most important subpopulation is CD4+CD25+Treg, which plays a role in maintaining autoimmune tolerance and The characteristic marker of Treg is the transcription factor FoxP3, the most important transcription factor controlling Treg phenotype and function [4], which influences the conversion of CD4+ T lymphocytes into regulatory T lymphocytes. In addition to suppressing T cells, Treg can also suppress dendritic cells and macrophages [5]. Although there are many other mechanisms, such as anti-inflammatory effects through cytotoxic T cell-mediated antigens, regulatory T lymphocytes exert their anti-inflammatory effects mainly through IL-10 or TGF-β. The following mechanisms of Treg action have been identified: (1) inhibition of co-stimulatory factors CD80 and CD86 expression, which in turn affects the maturation and function of dendritic cells. (2) Production of inhibitory cytokines such as IL-10 and TGF-β [6]. (3) Killing other immune cells through the granzyme-B and perforin pathways. In addition, it is now believed that adenosine produced by extracellular ATP can inhibit IL-6 expression while promoting TGF-β secretion [7], thereby inhibiting the production of effector T cells and enhancing Treg proliferation. 3, Role of regulatory T lymphocytes in hypertension The sluggish immune monitoring caused by abnormal number or function of regulatory T cells will contribute to the onset and development of inflammation, which is the pathophysiology of regulatory T cell involvement in hypertension. To investigate the influence of genetic factors on the inflammatory response to hypertension [8], Cowley et al. studied chromosomal substitution rats, which involves the introduction of chromosome 2 from brown Norway (BrownNorway) rats with normal blood pressure into SS rats with a genetic predisposition to hypertension [9], chromosome 2 carries a variety of pro-inflammatory genes (vascular cell adhesion molecule-1, IL-2, IL-6 receptor, fibroblast growth factor 2, angiotensin AT1b receptor) [10]. It was found that in SSBN2 rats, CD4+CD25+ and CD8+CD25+ lymphocytes and their expression product Foxp3 were increased, and low levels of regulatory T cells expressing FoxP3b as well as IL-10 were detected in the blood of Dahl SS rats. accompanied by an upregulated inflammatory response, vascular remodeling and dysfunction occurred in Dahl SS rats. Due to the inflammatory response of the vasculature, Dahl SS rats produced excessive amounts of pro-inflammatory cytokines such as IL-1, IL-2, IL-6, and TGF-β than chromosome-substituted rats. it was therefore concluded that the chromosome-2-dependent imbalance of anti-inflammatory and pro-inflammatory and immune responses favored the inflammatory response in genetically hypertensive rats and that the anti-inflammatory gene in Dahl SS rats was derived from SS brown Norway rats from chromosome 2. This imbalance in pro-inflammatory-anti-inflammatory cytokine responses was also found in T cells cultured in vitro, suggesting that it is at least partially independent of hypertension levels [9]. Transfer of regulatory T cells to Ang II-injected rats resulted in reduced systolic blood pressure, small arteriosclerosis, peroxide production, and a significant reduction in immune cell infiltration in vascular and perivascular tissues, along with the discovery of inflammatory mediators and immune cells in the cortical layer of the kidney [11]. Recent studies have shown that small arterial remodeling, oxidative stress and infiltration of immune cells in the vasculature and kidney were significantly reduced in mice injected with peroxisome, although the response to acquired regulatory T cells was not altered in blood pressure [12]. Thus, regulatory T cells as well as effector T lymphocytes are involved in the pathophysiology of hypertension, and they are also involved in the development and progression of other cardiovascular diseases [13-18]. Although additional mechanisms may be involved, regulatory T cells act mainly through the anti-inflammatory factor IL-10 [7,17,18]. In wild-type rats, infusion of Ang II induces only mild vascular endothelial dysfunction, but in IL-10-deficient rats, the increase in peroxides significantly affects the muscle relaxing effects of acetylcholine, suggesting that IL-10 production by regulatory T cells attenuates the production of reactive oxygen species in the vessel wall [19]. Transfer of regulatory T cells to Ang II-injected IL-10-deficient rats resulted in reduced systolic blood pressure and NADPH oxidase activity and improved vascular endothelial dysfunction [20]. Thus, IL-10 produced by regulatory T cells may improve vascular endothelial dysfunction with lower blood pressure by reducing NADPH oxidase activity. Activated CD4+CD25+ T cells inhibit T cell activation and proliferation mainly by contact inhibition and, in addition, by secreting the cytokines IL-10 and transforming growth factor-β (TGF-β).Barhoumi et al [21], by giving intermittent injections of CD4+CD25+ regulatory T cells or effector T cells to 12-month-old rats found that angiotensin-II somehow induced hypertension through adaptive immunity as well as regulatory mechanisms of effector T lymphocytes, that regulatory T lymphocytes were able to suppress effector T lymphocytes, and that the transcription factor Foxp3 was increased almost 2-fold by the peripatetic transfer of regulatory T cells compared to controls. Thus, to some extent, regulatory T lymphocytes were able to suppress angiotensin-II-mediated vascular damage through anti-inflammatory effects, confirming the involvement of immune mechanisms in angiotensin-II-induced blood pressure elevation, peroxidative stress in blood vessels, inflammation, and endothelial dysfunction. To investigate the effect of immunosuppressive effects of Treg on Ang II-related hypertension, Kvakan et al [22] transplanted Treg into Ang II-infiltrated rats and found no significant difference in blood pressure compared to controls (Ang II infiltration only), but improved cardiac hypertrophy as well as pathological changes in myocardial fibrosis and a significant reduction in inflammatory infiltration in the heart, suggesting that the cardioprotective independent of the effect on blood pressure regulation. The study also found that the number of activated T cells in the experimental and control groups was similar, presumably due to the activation of immune cells in the myocardium and the inhibition of migration of activated T lymphocytes from peripheral lymph nodes to the heart by Treg. Another important finding of this experiment is that Treg also caused electrical remodeling of the heart, mainly manifested by a reduced incidence of ventricular tachycardia. This experiment re-emphasizes the involvement of immune factors in the development and progression of hypertension, suggesting that immunomodulation may be a new idea for the treatment of hypertension. To investigate the relationship between regulatory T cells and gestational hypertension, Polanezyk et al [23] explored changes in circulating regulatory T cells in normal pregnant women and found that circulating system regulatory T cells were reduced during gestation and significantly decreased after delivery. CD4+CD25+ regulatory T cells in normal pregnant mice reduced the secretion and proliferation of lymphocyte interferon-γ (IFN-γ) in aborted mice [24], suggesting that regulatory T cells play a key role in the mechanism of allograft (fetal) tolerance, and that imbalance in immune rejection and immune tolerance leads to the development of other pregnancy comorbidities such as gestational hypertension, predicting that regulatory T cell number and function play an important role in the pathogenesis of hypertensive disorders in pregnancy [25]. To observe the relationship between the number of CD4+CD25+ T cells with immunosuppressive effects and the development of preeclampsia in gestational hypertension. Li Jia Ni et al [26] took 50 ul of anticoagulated venous blood from 30 patients with preeclampsia and performed flow cytometry analysis to determine the number of CD4+CD25+ T cells and the proportion of lymphocytes. The results revealed a decrease in the number of CD4+CD25+ T cells in patients with preeclampsia with hypertension during pregnancy. The maintenance of a normal pregnancy depends on the balance of immune rejection and immune tolerance. An increasing number of studies have confirmed that regulatory CD4+CD25+ T cells are elevated in human pregnancy[27-29]; some studies have also confirmed that regulatory CD4+CD25+ T cells can prevent abortion in mice due to immune rejection[27,30], and although such experimental studies have not been applied to human pregnancy, it is not difficult to infer that regulatory cells are involved in maternal-fetal immune tolerance[31,32] . . The decrease in the number of regulatory CD4+CD25+ T cells and the loss of maintenance of normal immune tolerance may be the mechanism by which regulatory T cells are involved in gestational hypertension. 4, Conclusion More and more studies have shown that regulatory T cells are involved in the occurrence and development of hypertension, and people gradually recognize the immune and inflammatory characteristics of hypertension, but we still need to study the pathophysiological mechanisms of regulatory T cells leading to hypertension in depth, so as to propose new effective treatments for hypertension and improve the prognosis of hypertension and cardiovascular diseases.