ROLE OF MONOCYTES IN AIDS AND AS TARGETS FOR ANTIVIRAL THERAPY

单核细胞和巨噬细胞在其表面表达cd4，是靶细胞。 治疗艾滋病病毒。吞噬细胞的感染没有细胞毒性，这些 慢性感染的细胞可能是艾滋病毒的蓄水池。续 这种人群的功能异常的特征是 对于了解艾滋病患者的免疫抑制状态是必不可少的。 最近的研究表明，艾滋病毒感染会诱导生产。 单核细胞和巨噬细胞特有的细胞因子：白介素1 受体拮抗剂(IL-1ra)。这种细胞因子是由激活的 吞噬细胞与IL-1受体结合，但不传递信号。 IL-1ra的独特之处在于它是已知的唯一内源性受体 对抗者。通过与IL-1受体结合，IL-1ra可减弱 IL-1的炎症作用。单核细胞同时产生IL-1和IL-1ra， 而这两种细胞因子之间的关系对于 维持免疫细胞募集/激活之间的适当平衡 免疫抑制和组织修复。除了影响 免疫状态，感染的单核细胞是HIV-1的储备者，有利于 针对这一人群的选择性治疗目标。HIV-1病毒的相互作用 随着细胞表面的CD4转导信号诱导分泌 细胞因子，以及激活抗原的从头表达。为 例如，HIV+个体的单核细胞可能是CD16+和IL-2R+。 对照受试者的单核细胞。白介素2受体的出现 被感染的细胞为靶向毒素提供了基础。当前的研究 正专注于抗原表达的其他变化和 表面受体作为选择性毒素靶点用于治疗 干预。

Monocytes and macrophages express CD4 on their surface and are targets for HIV. Infection of phagocytic cells is not cytotoxic, and these chronically infected cells may serve as a reservoir for HIV. Continued characterization of the functional abnormalities of this population is essential to understanding the immunosuppressed state of AIDS patients. Recent studies have demonstrated that HIV infection induces production of a cytokine unique to monocytes and macrophages: the interleukin-1 receptor antagonist (IL-1ra). This cytokine is secreted by activated phagocytes, binds to the IL-1 receptor, but does not transduce a signal. IL-1ra is unique in that it is the only known endogenous receptor antagonist. By binding to the IL-1 receptor, IL-1ra attenuates the pro- inflammatory actions of IL-1. Monocytes produce both IL-1 and IL-1ra, and the relationship between these two cytokines is crucial to maintaining the proper balance between immune cell recruitment/activation and immunosuppression and tissue repair. In addition to influencing immune status, infected monocytes serve as a reservoir for HIV-1 favoring selective therapeutic targeting of this population. Interaction of HIV-1 with cell surface CD4 transduces a signal inducing secretion of cytokines, and also de novo expression of activation antigens. For example, monocytes from HIV+ individuals maybe CD16+ and IL-2R+ in contrast to monocytes from control subjects. The emergence of IL-2R on infected cells provides the basis for targeted toxins. Current studies are focusing on other alterations in the expression of antigens and surface receptors as selective toxin targets for therapeutic intervention.