Regulatory T cells and cardiovascular diseases

Abstract

Inflammation is a major underlying mechanism in the progression of numerous cardiovascular diseases (CVDs). Regulatory T cells (Tregs) are typical immune regulatory cells with recognized immunosuppressive properties. Despite the immunosuppressive properties, researchers have acknowledged the significance of Tregs in maintaining tissue homeostasis and facilitating repair/regeneration. Previous studies unveiled the heterogeneity of Tregs in the heart and aorta, which expanded in CVDs with unique transcriptional phenotypes and reparative/regenerative function. This review briefly summarizes the functional principles of Tregs, also including the synergistic effect of Tregs and other immune cells in CVDs. We discriminate the roles and therapeutic potential of Tregs in CVDs such as atherosclerosis, hypertension, abdominal arterial aneurysm, pulmonary arterial hypertension, Kawasaki disease, myocarditis, myocardial infarction, and heart failure. Tregs not only exert anti-inflammatory effects but also actively promote myocardial regeneration and vascular repair, maintaining the stability of the local microenvironment. Given that the specific mechanism of Tregs functioning in CVDs remains unclear, we reviewed previous clinical and basic studies and the latest findings on the function and mechanism of Tregs in CVDs.

Trained Innate Immunity in Animal Models of Cardiovascular Diseases

“…There is a large body of evidence that T cell and B cell responses impact on cardiovascular diseases [66][67][68] and that there is a crosstalk between innate as well as adaptive immune responses during their initiation and progression [69,70]. If and how trained innate immunity engages in this process is currently also unclear.…”

Effects and mechanisms of the myocardial microenvironment on cardiomyocyte proliferation and regeneration

“…According to their phenotypes, cytokine expression profiles, and functions, CD4 + T cells can be further divided into T helper type 1 (Th1), T helper type 2 (Th2), and regulatory T-cell (Treg) subsets ( Hofmann et al, 2012 ). The mechanism of T-cell stimulated cardiac regeneration response is currently unclear, and it is likely to be multifactorial, involving communication between several cell types (USSCs, immune cells, T cells, and hypoxic cardiomyocytes), as well as paracrine regenerative factors ( Hu et al, 2023 ).…”