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首页> 外文期刊>Cytokine >IL-12 plays a significant role in the apoptosis of human T cells in the absence of antigenic stimulation.
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IL-12 plays a significant role in the apoptosis of human T cells in the absence of antigenic stimulation.

机译：在没有抗原刺激的情况下，IL-12在人类T细胞的凋亡中起着重要作用。

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摘要

Interleukin-12 (IL-12) is an immunoregulatory cytokine that plays an essential role in cell-mediated immunity. It is known to induce T cell apoptosis in in vivo systems such as graft-versus-host disease (GVHD) and experimental autoimmune uveitis (EAU). However, the role of IL-12 in T cell apoptosis in the absence of antigenic stimulation has not been clearly defined. This study was conducted to investigate whether IL-12, in the absence of an antigen, is able to induce T cell apoptosis, and also, which signalling pathways utilized by IL-12 are involved in this process. Our data clearly showed that IL-12 in the absence of an antigen induces apoptosis in T cells. Flow cytometry and ELISA showed FasL up-regulation and increased IFN-gamma synthesis in IL-12 treated T cells, while Fas and TNF-R1 showed little change. Semi-quantitative RT-PCR demonstrated that IL-12 was able to up-regulate TNF-alpha and FasL mRNA expression. Furthermore, IL-12 induced apoptosis was associated with caspase-3, caspase-2, caspase-7, DNA fragmentation factor 45 (DFF45) and Fas associated death domain (FADD) whereas TNF receptor associated death domain (TRADD) and receptor interacting protein (RIP) were not. Inhibition of Janus tyrosine kinase (JAK) was able to suppress IL-12 induced T cell apoptosis. Anti-FasL antibody was able to block IL-12 induced T cell apoptosis. In conclusion, our findings suggest that IL-12 is able to induce T cell apoptosis in the absence of an antigen. In addition, the present data suggest that this process is FasL mediated and caspase-3 dependent. Furthermore, JAK was shown to be involved in this process. These results may have significant implications in the understanding of IL-12 mediated T cell apoptosis.
机译：白细胞介素12（IL-12）是一种免疫调节细胞因子，在细胞介导的免疫中起重要作用。已知在诸如移植物抗宿主病（GVHD）和实验性自身免疫性葡萄膜炎（EAU）的体内系统中诱导T细胞凋亡。然而，在没有抗原刺激的情况下，IL-12在T细胞凋亡中的作用尚未明确。进行该研究以调查在没有抗原的情况下IL-12是否能够诱导T细胞凋亡，以及该过程中涉及IL-12所利用的哪些信号通路。我们的数据清楚地表明，没有抗原的IL-12会诱导T细胞凋亡。流式细胞仪和ELISA显示IL-12处理的T细胞中FasL上调并增加IFN-γ合成，而Fas和TNF-R1几乎没有变化。半定量RT-PCR显示IL-12能够上调TNF-α和FasL mRNA的表达。此外，IL-12诱导的凋亡与caspase-3，caspase-2，caspase-7，DNA断裂因子45（DFF45）和Fas相关死亡域（FADD）相关，而TNF受体相关死亡域（TRADD）和受体相互作用蛋白（RIP）没有。抑制Janus酪氨酸激酶（JAK）能够抑制IL-12诱导的T细胞凋亡。抗FasL抗体能够阻断IL-12诱导的T细胞凋亡。总之，我们的发现表明，IL-12能够在没有抗原的情况下诱导T细胞凋亡。此外，目前的数据表明该过程是FasL介导的和caspase-3依赖性的。此外，已证明JAK参与了此过程。这些结果可能对理解IL-12介导的T细胞凋亡具有重要意义。

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