Shearer G M, Clerici M
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
Pediatr Res. 1993 Jan;33(1 Suppl):S71-4; discussion S74-5. doi: 10.1203/00006450-199305001-00410.
The severe depletion of CD4+ T cells is the most obvious and dramatic immunologic event that occurs in individuals infected with the human immunodeficiency virus (HIV) type 1 during development to AIDS. Nevertheless, a complex and sequential pattern of loss of T-helper cell (TH) function can occur years before development of AIDS symptoms. Such suppression could be due to immunosuppressive factors that are either products of HIV, such as gp120 and tat, or HIV-induced immunoregulatory cytokines such as transforming growth factor-beta and IL-10. Recent data suggest that multiple and independent immunosuppressive factors, including gp120-induced suppression and IL-10, are responsible for the loss of TH function seen in HIV-infected individuals before development of symptoms. The same TH functional abnormalities observed in adult patients are also seen in pediatric cases. Pediatric cases of HIV infection present some unique problems, however, in that one needs to be able to distinguish between HIV-induced suppression of TH function and the absence of TH function that is due to lack of maturation or immunologic priming.
在1型人类免疫缺陷病毒（HIV）感染个体发展为获得性免疫缺陷综合征（AIDS）的过程中，CD4 + T细胞的严重耗竭是最明显且显著的免疫学事件。然而，在AIDS症状出现前数年，T辅助细胞（TH）功能可能会出现复杂且循序渐进的丧失模式。这种抑制可能是由于免疫抑制因子导致的，这些因子要么是HIV的产物，如gp120和tat，要么是HIV诱导的免疫调节细胞因子，如转化生长因子-β和白细胞介素-10。最近的数据表明，多种独立的免疫抑制因子，包括gp120诱导的抑制和白细胞介素-10，是导致HIV感染个体在出现症状前TH功能丧失的原因。在成年患者中观察到的相同TH功能异常在儿科病例中也可见。然而，儿科HIV感染病例存在一些独特问题，即需要能够区分HIV诱导的TH功能抑制与由于缺乏成熟或免疫启动导致的TH功能缺失。
