《生命科学》 2016, 28(4): 498-503

调节性T细胞亚群与动脉粥样硬化关系的研究进展

杨飞飞1，王嘉军2*

(1 三峡大学医学院，宜昌 443002；2 湖北民族学院医学院，恩施 445000)

摘　要：摘　要：动脉粥样硬化(atherosclerosis， AS) 是目前威胁人类健康的主要病变之一。AS 作为一种脂质代谢异常诱导的大、中动脉血管壁慢性炎症性疾病，其主要表现为大量脂质沉积到血管壁，并伴随多种免疫细胞浸润及平滑肌细胞增生。AS 的发病机制尚未明确。目前认为，炎症在动脉粥样硬化的发生发展过程中发挥了重要的作用。特异和非特异性免疫反应均参与了此疾病的发展过程。近几年研究发现，调节性T 细胞(regulatory T cells， Treg) 介导的免疫抑制效应在AS 的发生发展中发挥重要作用。Treg 细胞是一类具有独特
    免疫调节功能的CD4+ T 细胞亚群，包括CD4+CD25+ Treg 细胞、1 型调节性T 细胞(type 1 regulatory T cells， Tr1)、3 型辅助性T 细胞(type 3 helper T cell， Th3) 和CD4+LAP+ Treg 细胞等。现就这4 种主要的Treg 细胞亚群的特点、与动脉粥样硬化发生发展的关系及可能的作用机制作一综述。

The role of regulatory T cell subsets in atherosclerosis

YANG Fei-Fei1， WANG Jia-Jun2*

(1 Medical College of China Three Gorges University， Yichang 443002， China; 2 Medical College of Hubei Institute for Nationalities， Enshi 445000， China)

Abstract: Abstract: Atherosclerosis (AS) is one of the major diseases that endanger human health at present. As a kind of chronic inflammatory disease of large- and medium-sized arteries induced by abnormal lipid metabolism， the main embodiment of AS is the deposition of a large amount of lipid in the vessel and accompanying infiltration of many immune cells and proliferation of smooth muscle cells. The exact mechanism about the pathogenesis of AS is still unclear. At present， inflammation is considered to be the main factor for the development of atherosclerosis. Both specific and nonspecific immunity are involved in the development of this disease. More and more evidence shows that immunosuppressed effect mediated by regulatory T cells (Treg) plays an important role in the occurrence and development of AS. Treg cells as a unique T cell subset， could be divided into different subgroups， including CD4+CD25+ Treg， type 1 regulatory T cells (Tr1)， type 3 helper T cell (Th3)， CD4+LAP+ Treg cells and so on. Researches about relationship between Treg cell subsets and AS are increasing in recent years. In this paper， we give a review about characteristics of different Treg cell subgroups and the association between Treg cells and AS as well as the possible pathogenic mechanism.