Kinter A, Fauci A S
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md, USA.
Immunol Res. 1996;15(1):1-15. doi: 10.1007/BF02918280.
A hallmark of human immunodeficiency virus (HIV) infection is the progressive loss of CD4+ T lymphocytes; however, qualitative defects in immune responses occur prior to the precipitous drop CD4+ T cell numbers. One of the first immunologic defects to be described in HIV-infected individuals is a deficiency in interleukin (IL)-2 production. The addition of IL-2 in vitro to cultures of mononuclear cells from HIV-infected individuals partially or completely restored certain defective cellular immune responses. However, production of or addition of IL-2 has also been associated with increased viral replication in infected T cells. These observations underscore the pernicious correlation between immune activation and HIV replication. However, recent in vitro and in vivo studies have provided promising preliminary results suggesting that, at least at certain stages of disease, the benefits of IL-2 mediated immune enhancement may outweigh or override the inductive effects of this cytokine on HIV production.
人类免疫缺陷病毒（HIV）感染的一个标志是CD4+ T淋巴细胞的逐渐丧失；然而，免疫反应的质量缺陷在CD4+ T细胞数量急剧下降之前就已出现。在HIV感染者中首先被描述的免疫缺陷之一是白细胞介素（IL）-2产生不足。在体外将IL-2添加到HIV感染者的单核细胞培养物中，可部分或完全恢复某些有缺陷的细胞免疫反应。然而，IL-2的产生或添加也与受感染T细胞中病毒复制增加有关。这些观察结果强调了免疫激活与HIV复制之间的有害关联。然而，最近的体外和体内研究提供了有希望的初步结果，表明至少在疾病的某些阶段，IL-2介导的免疫增强的益处可能超过或抵消这种细胞因子对HIV产生的诱导作用。
