Regulatory T cells in cardiovascular diseases

Abstract

Inflammation is essential in the initial development and progression of many cardiovascular diseases involving innate and adaptive immune responses. The role of CD4(+)CD25(+)FOXP3(+) regulatory T (TREG) cells in the modulation of inflammation and immunity has received increasing attention. Given the important role of TREG cells in the induction and maintenance of immune homeostasis and tolerance, dysregulation in the generation or function of TREG cells can trigger abnormal immune responses and lead to pathology. A wealth of evidence from experimental and clinical studies has indicated that TREG cells might have an important role in protecting against cardiovascular disease, in particular atherosclerosis and abdominal aortic aneurysm. In this Review, we provide an overview of the roles of TREG cells in the pathogenesis of a number of cardiovascular diseases, including atherosclerosis, hypertension, ischaemic stroke, abdominal aortic aneurysm, Kawasaki disease, pulmonary arterial hypertension, myocardial infarction and remodelling, postischaemic neovascularization, myocarditis and dilated cardiomyopathy, and heart failure. Although the exact molecular mechanisms underlying the cardioprotective effects of TREG cells are still to be elucidated, targeted therapies with TREG cells might provide a promising and novel future approach to the prevention and treatment of cardiovascular diseases.

Neutrophils induce proangiogenic T cells with a regulatory phenotype in pregnancy

“…FOXO1 is a known important transcription factor that promotes FOXP3 expression in T cells; however, FOXO1 has broader implications in placentation and indeed is necessary for normal placental development, as indicated by the abnormalities observed in FOXO1-null mice (38). Similarly, the role of Tregs in pregnancy might not be confined to regulating immune responses; broader effects of Tregs on the maternal vasculature have been reported, with downstream relevance in controlling hypertension and other cardiovascular events (53). Moreover, Tregs can modulate cell surface proteins on endothelial cells, leading to an anti-inflammatory endothelial cell phenotype (54).…”

Hypoxia-Inducible Factor Prolyl 4-Hydroxylase-2 Inhibition Protects Against Development of Atherosclerosis

“…29 Because Tregs, and the suppressive cytokines produced by them, have been implicated in atherosclerosis protection, pharmacological HIF-P4H-2 inhibition may further diminish vascular inflammation by inducing them. 30 More recently, HIF-1α-driven optimization of carbohydrate metabolism, also acquired with a nonspecific 2-oxoglutarate inhibitor analogue DMOG, during an inflammatory acute lung injury, provided lung protection and dampened inflammation. 31 The data available suggest that HIFα stabilization via HIF-P4H inhibition can modulate immunologic responses, making them potential therapeutic targets in the treatment of chronic inflammatory diseases.…”

Change of Peripheral Blood Treg/Thl7 in Cognitive Impairment with Chronic Renal Failure Patients

“…These cells account for 5–10% of the peripheral CD4 + T cells and are responsible for inducing and maintaining immune homeostasis and resistance [6]. Regulatory T cells can be divided into natural Treg (nTreg) cells and inducible Treg (iTreg) cells, and they express CD25, CD39, CTLA-4 and Foxp3, as well as other molecules [6].…”

“…These cells account for 5–10% of the peripheral CD4 + T cells and are responsible for inducing and maintaining immune homeostasis and resistance [6]. Regulatory T cells can be divided into natural Treg (nTreg) cells and inducible Treg (iTreg) cells, and they express CD25, CD39, CTLA-4 and Foxp3, as well as other molecules [6]. NTreg cells can significantly inhibit the proliferation of dendritic cells (DCs), monocytes, CD4 + T cells and CD8 + T cells by direct modulation of CTLA4 and other cell membrane inhibitory molecules that are in direct contact with effector cells.…”