影响和干预人类白细胞抗原(HLA)在宿主细胞表面表达是病毒逃避机体抗病毒免疫的重要途径之一。人类白细胞抗原G(HLA-G)是机体内一个重要的免疫耐受分子,多种病毒感染后均可诱导HLA-G分子的表达,促进病毒的免疫逃逸。在人类免疫缺陷病毒(HIV)感染过程中,HIV可通过多种机制诱导HLA-G分子在单核细胞、T淋巴细胞表面的异常表达及分泌大量可溶性HLA-G(sHLA-G)。HIV诱导表达的HLA-G分子与其受体结合,通过直接抑制NK细胞、T淋巴细胞等免疫细胞的生物学活性或间接诱导HLA-G+Treg发挥免疫抑制功能,使HIV病毒有效逃避宿主的免疫监视及攻击。本文就HLA-G结构、受体、基因多态性与HIV易感性、HIV感染与HLA-G分子异常表达,和HLA-G对免疫细胞的影响等作一综述。 Influencing and intervening the expression of human leukocyte antigen (HLA) on the surface of host cells is one of the important ways to evade virus antiviral immunity. Human Leukocyte Antigen G (HLA-G) is an important immune tolerance molecule in the body. All kinds of virus can induce the expression of HLA-G and promote the immune escape. In the process of human immunodeficiency virus (HIV) infection, HIV can induce the abnormal expression of HLA-G molecules on the surface of monocytes and T lymphocytes by a variety of mechanisms and secrete large amounts of soluble HLA-G (sHLA-G). HIV-induced expression of HLA-G molecules bind to their receptors, and can effectively evade host immunity by directly inhibiting the biological activity of immune cells such as NK cells and T lymphocytes or indirectly inducing immunosuppressive function of HLA-G + Tregs Surveillance and attack. This review summarizes the effects of HLA-G structure, receptor, gene polymorphism and HIV susceptibility, HIV infection and the abnormal expression of HLA-G molecules, and HLA-G on immune cells.