The mechanism and research progress of T lymphocyte-mediated immune response in cardiac fibrosis remodeling.
- Author:
Yong PENG
1
;
Wen-Yue GAO
2
;
Di QIN
2
Author Information
1. Jiangsu Collaborative Innovation Center for Sports and Health Project, Nanjing Sport Institute, Nanjing 210014, China.
2. School of Sport Health, Nanjing Sport Institute, Nanjing 210014, China.
- Publication Type:English Abstract
- MeSH:
Humans;
Fibrosis;
T-Lymphocytes, Regulatory/immunology*;
Ventricular Remodeling/immunology*;
Myocardium/immunology*;
Animals;
Th17 Cells/immunology*;
Interleukin-10/metabolism*;
Th1 Cells/immunology*;
Th2 Cells/immunology*
- From:
Acta Physiologica Sinica
2025;77(1):95-106
- CountryChina
- Language:Chinese
-
Abstract:
This article reviews the role of different types of T lymphocyte subpopulations in pathological cardiac fibrosis remodeling. T helper 17 (Th17) cells are implicated in promoting the development of pathological cardiac fibrosis remodeling, while regulatory T (Treg) cells exert an immunosuppressive functions as negative regulators, attributing to their interleukin-10 (IL-10) secretion and functional phenotype. Th1 and Th2 cells are involved in different stages of the inflammatory response in pathological cardiac fibrosis remodeling, and their influence varies according to the pathological mechanisms of different cardiac diseases. In addition, CD8+ T cells regulate the activation and polarization of macrophages, promote the secretion of granzyme B, induce cardiomyocyte apoptosis, and aggravate cardiac fibrosis post-myocardial infarction. Considering the limitation of cytokine modulation in clinical therapy of heart failure, targeting T-cell co-stimulatory molecules emerges as a promising strategy for treating pathologic cardiac remodeling. Future research will explore chimeric antigen receptor modified T cells (CAR-T cells) technology and targeted regulation of Treg cells quantity and phenotype, for both of which have the potential to become effective methods for treating heart disease.
