HIV和结核分枝杆菌共同感染的免疫学机制

发布时间：2018-06-05 17:51

本文选题：人类免疫缺陷病毒 + 结核分枝杆菌　；参考：《中国艾滋病性病》2014年04期

【摘要】：人类免疫缺陷病毒(HIV)和结核分枝杆菌共感染是全球性公共卫生重大问题,结核分枝杆菌和HIV均是在细胞内复制的病原体,通过损伤细胞免疫而造成持续感染。随着免疫学的进展,人们逐渐了解HIV和结核分枝杆菌共感染的一些临床特点及免疫学机制。树突状细胞(DCs)通过高水平表达主要组织相容性复合物II(MHC II)类分子、协同分子及黏附分子,诱导免疫激活,促使T细胞增殖。HIV和结核分枝杆菌感染后树突状细胞功能受损,导致Th1/Th2及Treg/Th17(help T cell,辅助性T细胞;Regulatery T cell,调节性T细胞)平衡打破,进一步降低了细胞毒性T细胞(CTL)清除结核分枝杆菌和HIV的能力。随着HIV和结核分枝杆菌共感染免疫机制研究的不断深入,人们对HIV合并结核分枝杆菌感染的诊治水平将不断提高。
[Abstract]:Human immunodeficiency virus (HIV) and Mycobacterium tuberculosis co-infection are major global public health problems. Both Mycobacterium tuberculosis and HIV are the pathogens that replicate in cells and cause persistent infection by damaging cellular immunity. With the development of immunology, some clinical features and immunological mechanisms of co-infection of HIV and Mycobacterium tuberculosis have been gradually understood. Dendritic cells (DCs) express the major histocompatibility complex (II(MHC II) class molecules at high level, which can induce immune activation by synergistic molecules and adhesion molecules, and impair the function of dendritic cells after infection with T cell proliferation and Mycobacterium tuberculosis. As a result, the balance of Th1/Th2 and Treg/Th17(help T cells (helper T cells, regulatory T cells) was broken, and the ability of cytotoxic T cells to eliminate Mycobacterium tuberculosis and HIV was further decreased. With the further study of the immune mechanism of HIV and Mycobacterium tuberculosis co-infection, the level of diagnosis and treatment of HIV with Mycobacterium tuberculosis infection will be improved.
【作者单位】：华山医院感染科;
【基金】：上海市医学引导类项目(124119a6400) 高等学校博士专项科研基金(20110071110068)~~
【分类号】：R512.91;R378.911

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