TYPE-1 TYPE-2 CYTOKINE MODULATION OF T-CELL PROGRAMMED CELL-DEATH AS A MODEL FOR HUMAN-IMMUNODEFICIENCY-VIRUS PATHOGENESIS
TYPE-1 TYPE-2 CYTOKINE MODULATION OF T-CELL PROGRAMMED CELL-DEATH AS A MODEL FOR HUMAN-IMMUNODEFICIENCY-VIRUS PATHOGENESIS
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DOI：
10.1073/pnas.91.25.11811
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发表时间：
1994-12-06
影响因子：
11.1
通讯作者：
HENKART, PA
中科院分区：
文献类型：
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作者：
CLERICI, M;SARIN, A;HENKART, PA
在体外T细胞受体诱导的程序性细胞死亡的激活T细胞从人类免疫缺陷病毒血清阴性（HIV-）的捐助者和静息T细胞从HIV+捐助者的细胞因子的影响很大。加入外源性重组“1型”淋巴因子干扰素γ和白细胞介素2（IL-2）以及巨噬细胞产生的IL-12（有利于细胞介导的T细胞应答），可阻断T淋巴细胞程序性细胞死亡的两个系统。相比之下，“2型”淋巴因子IL-4和IL-10，这有利于抗体反应，要么没有效果，要么增强这些系统的体外T细胞程序性细胞死亡。在含有单核细胞的培养物中，抗IL-4和IL-10抗体抑制T细胞受体介导的死亡，抗IL-12抗体增强T细胞受体介导的死亡，提示内源性产生的细胞因子的作用。这些结果表明，1型和2型细胞因子类的功能特性可以进一步扩展到包括它们对T细胞程序性细胞死亡的影响以及它们在HIV感染的发病机制中的可能作用。
In vitro T-cell receptor-induced programed cell death in both activated T cells from human immunodeficiency virus-seronegative (HIV-) donors and resting T cells from HIV+ donors was substantially influenced by cytokines. Addition of exogenous recombinant ''type 1'' lymphokines interferon gamma and interleukin 2 (IL-2), as well as the macrophage-produced IL-12, which favor cell-mediated T-cell responses, blocks both systems of T-lymphocyte programed cell death. In contrast, the ''type 2'' lymphokines IL-4 and IL-10, which favor antibody responses, either had no effect or enhanced these systems of in vitro T-cell programed cell death. A role for endogenously produced cytokines was suggested by the inhibition of T-cell receptor-mediated death by antibodies against IL-4 and IL-10 and its enhancement by anti-IL-12 in cultures containing monocytes. These results demonstrate that the functional properties of type 1 and type 2 cytokine classes may be further extended to include their effects on T-cell programed cell death and their possible role in the pathogenesis of HIV infection.