Arndt R, Keeser D
Z Hautkr. 1989 May 15;64(5):353-4, 357-8, 363.
CD4 + T-helper lymphocytes are the main target cells in HIV infection. Since CD4 molecules are not restricted to T-cells but also found on monocytes, macrophages, follicular dendritic cells, Langerhans cells, and microglial brain cells, these cells might be affected, too, by HIV. HIV binds via the gp 120 envelope protein to the 67 KD CD4 membrane protein. Patients with HIV infection show distinct autoimmunological reactions against the cells of their immune system. Autoantibodies directed against CD4 cells seem to be responsible for the extent of the immune deficiency and are, therefore, of prognostic value. Aside from CD4+ cell depletion, the functional impairment of the T-cell system plays an important part in the progress of the disease. Patients with depressed gamma-interferon production after stimulation with antigens are at a risk for AIDS-related opportunistic infections. Polyclonal production of immunoglobulins and impaired stimulation of B-cells are characteristic for B-cell dysfunction. NK-cell dysfunction depends on reduced production of IL-2 and altered gamma-interferon production of T-cells infected with HIV.
CD4 + T辅助淋巴细胞是HIV感染的主要靶细胞。由于CD4分子不仅存在于T细胞上，也存在于单核细胞、巨噬细胞、滤泡树突状细胞、朗格汉斯细胞和脑小胶质细胞上，这些细胞也可能受到HIV的影响。HIV通过gp 120包膜蛋白与67 KD的CD4膜蛋白结合。HIV感染患者对其免疫系统细胞表现出明显的自身免疫反应。针对CD4细胞的自身抗体似乎决定了免疫缺陷的程度，因此具有预后价值。除了CD4 +细胞耗竭外，T细胞系统的功能损害在疾病进展中起重要作用。抗原刺激后γ干扰素产生受抑制的患者有发生艾滋病相关机会性感染的风险。免疫球蛋白的多克隆产生和B细胞刺激受损是B细胞功能障碍的特征。NK细胞功能障碍取决于IL - 2产生减少以及感染HIV的T细胞γ干扰素产生改变。
