Targeting regulatory T cells for cardiovascular diseases

Abstract

Cardiovascular diseases (CVDs) are the leading cause of death and disability worldwide. The CVDs are accompanied by inflammatory progression, resulting in innate and adaptive immune responses. Regulatory T cells (Tregs) have an immunosuppressive function and are one of the subsets of CD4+T cells that play a crucial role in inflammatory diseases. Whether using Tregs as a biomarker for CVDs or targeting Tregs to exert cardioprotective functions by regulating immune balance, suppressing inflammation, suppressing cardiac and vascular remodeling, mediating immune tolerance, and promoting cardiac regeneration in the treatment of CVDs has become an emerging research focus. However, Tregs have plasticity, and this plastic Tregs lose immunosuppressive function and produce toxic effects on target organs in some diseases. This review aims to provide an overview of Tregs’ role and related mechanisms in CVDs, and reports on the research of plasticity Tregs in CVDs, to lay a foundation for further studies targeting Tregs in the prevention and treatment of CVDs.

Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction

“…Interferon-G + T-cells correlated with the NYHA functional class and serum brain natriuretic peptide levels in outpatients with heart failure [30]. Treg acts to resolve inflammation by secreting anti-inflammatory interleukin-10 [31] and inhibiting the activity of effector cells, including Th1 and macrophages [31,32]. In rodent models with angiotensin II infusion [33] or abdominal aortic constriction [24], the adoptive transfer of Treg reduced myocardial infiltration through macrophages and ameliorated cardiac hypertrophy and fibrosis.…”

Beyond the Granuloma: New Insights into Cardiac Sarcoidosis Using Spatial Proteomics

“…There is precedence for this theory, with publications on several cardiovascular and autoimmune diseases reporting an association between reduced Treg-to-effector T-cell ratio and pathologic in ammation. [53][54][55] This imbalance between the number of Tregs and the number of effector immune cells in in ammation(+) CS parenchyma is only revealed because of the spatial expression methods employed in this experiment. Non-spatially resolved expression methods which would 'average' the Treg expression across the tissue, would miss such subtleties in regional expression.…”

Cardiac fibrogenesis: an immuno-metabolic perspective

“…Moreover, they have been observed to secrete signals that inhibit fibrosis ( Tang et al, 2012 ); however, the precise characteristics of these signals have yet to be elucidated. Notably, T regs can secrete fibrous mediators, such as TGF-β ( Taylor et al, 2006 ; Saxena et al, 2014 ; Wang et al, 2023 ). Hence, the regulatory role of these cells in the fibrotic response is likely dependent on the specific circumstances and the balance between fibrotic and anti-fibrotic cellular processes.…”