动物实验,T细胞亚群 z-bo 2020-09-04 403

　　Cardiovascular disease is one of the leading causes of death in the world. According to the World Health Organization (WHO), about 20 million people died of cardiovascular disease in 2015, and it is still the leading cause of death in the world. Ventricular remodeling is the main reason why many heart diseases eventually develop into heart failure. In diseases such as hypertension, cardiomyopathy, valvular dysfunction, and myocardial infarction, long-term, uncontrolled hypertrophy due to various pathological stimuli (such as pressure and volume overload, sarcomere mutation and neurohumoral activation) Plastic. Occurrence, leading to heart failure, eventually leading to heart failure or cardiac arrest.

　　Recent studies have shown that during myocardial hypertrophy and remodeling, various inflammatory signal transduction pathways are changed and inflammatory cell activation caused by various causes. The inflammatory signal molecules released by the latter may trigger hypertrophy and fibrosis. Recent studies believe that the inflammatory response is mediated by immune cells that initially reside and are absorbed by the heart, before hypertrophy and cardiomyocyte remodeling, and persist throughout the ventricular remodeling process. Early inflammation can remove dead cells and help promote scar formation and prevent heart rupture. Excessive inflammation can cause extracellular matrix degradation and apoptosis, leading to ventricular remodeling and heart failure. .. In the past, it was thought that the inflammatory response after heart injury was related to the innate immune response mediated mainly by neutrophils, macrophages and dendritic cells. Recent studies have found that adaptive immune response plays a key role in ventricular remodeling, and chronic inflammation involving different T cell subgroups is closely related to the development of ventricular remodeling. .. It can induce natural T lymphocytes to differentiate into different T effector cell subgroups in different microenvironments and exhibit different functions. T cells are mainly divided into helper T cells, regulatory T cells and cytotoxic T cells. According to the expression and function of transcription factors, Th cells can be divided into Th1, Th2, Th17, Th22, Th9 and other subtypes. Different T cell subpopulations express different chemokine receptors, mediate the migration and recruitment of different T cell subpopulations, and T cells that migrate to the inflammatory area perform specific effector functions.

　　Research shows that T lymphocytes play an important role in the development of ventricular remodeling and heart failure. Recent studies have shown that T cells are recruited to the heart and participate in the pathophysiological process of ventricular remodeling in various heart diseases. For many reasons, knocking out mouse T lymphocytes can significantly improve ventricular weight. construction. In a mouse model of cardiac TNF-α overexpression, anti-CD3 antibodies can neutralize T cells, reduce the recruitment of inflammatory cells to the heart and prevent cardiac hypertrophy. In a model of myocardial hypertrophy caused by pressure overload, the degree of myocardial fibrosis in T cell-deficient Rag2 mice is reduced, and the infiltration of macrophages is reduced. Another study reported that Rag-1-deficient mice can alleviate vascular dysfunction caused by hypertension and angiotensin II, and T cells may be involved in cardiac hypertrophy and remodeling caused by hypertension.

　　Recent studies have shown that in a mouse model of diabetic cardiomyopathy, knocking out CD3 + T cells can improve heart function and reduce the degree of myocardial fibrosis. Further studies confirmed that T cell subsets, such as Th1, Th2, Th17 cells, Treg and killer T cells, play an important role in repairing myocardial injury and ventricular remodeling.