CD4^＋T淋巴细胞在炎症性心脏重构中的作用  

Progression in the study of CD4^ ＋ T cells inflammation mediated cardiac remodeling

作　　者：刘巍[1] 王雪婷[1] 冯微微[1] 

机构地区：[1]哈尔滨医科大学附属第一医院心内科,150001

出　　处：《国际免疫学杂志》2011年第3期198-200,共3页International Journal of Immunology

基　　金：黑龙江省教育厅科学技术研究项目（11531171）

摘　　要：心肌纤维化是指心肌细胞外基质进行性累积，导致心室僵硬和舒张充盈受损，是心衰患者临床预后不良的指标。多种原因导致的心肌纤维化均经历过炎症过程，炎症与心肌纤维化常并存于病变心肌。T淋巴细胞通过与心肌成纤维细胞相互作用而影响胶原及基质金属蛋白酶表达，参与炎症性心肌纤维化的调控。对于不同T淋巴细胞亚群如Th1、Th2、Th17细胞、CD4^＋CD25^＋调节性T细胞（Treg）对炎症性心肌纤维化的影响及机制的理解为心肌纤维化、心力衰竭的治疗提供新靶点。Cardiac fibrosis is defined as a progressive accumulation of fibrillar extracellular matrix （ECM） in cardiac tissue. The regulation of extracellular matrix remodeling is primarily mediated by cardiac fibroblasts （CF）. Evidences suggest that various T lymphocytes differentially affect organ fibrosis through modulating collagen and MMPs/TIMPs gene expression, MMPs activity and cardiac collagen cross-linking, leading to altered ECM composition. In this review, we will address the role of different T cell subsets in inflammation mediated cardiac fibrosis, from the perspective of T cells and fibroblasts interaction. We conclude that, in addition to preventive strategies, therapies based on deviation of Thl/Th2. paradigm, and manipulation of Tregs and Thl7 would show promising results in heart failure investigations in the future.

关 键 词：调节性T细胞 TH17细胞 TH1/TH2 成纤维细胞 心肌纤维化 

分 类 号：R54[医药卫生—心血管疾病]