HIV和结核分枝杆菌共同感染的免疫学机制

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。

The mechanisms of immune response to coinfection of tuberculosis and HIV

The epidemics of tuberculosis （TB） and Human immunodeficiency virus （HIV） coinfection have had deadly consequences around the world. Both Mycobacterium tuberculosis and HIV are pathogens replicated within host cells, resulting in persistent infection through impairing cellular immunity. With progress in immunology, clinical features and its immunological mechanisms of HIV/TB co-infection are gradually known. Dendritic cells induce immune activation and promote T cell proliferation by high expression of major histocompatibility complex （MH- CII）, co-stimulatory molecules and adhesion molecules. Functional impairment of Dendritic Cells （DCs） caused by HIV/TB coinfection would break the balance of Th1/Th2 and Treg/Th17 and furtherly weaken the ability of Cytotoxic T Lymphocyte （CTL） to clear TB and HIV. With the deep research on mechanisms of HIV/TB coinfection, the diagnosis and treatment of HIV/TB coinfection will he improved continuously.