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白细胞介素-1β、白细胞介素-6与肿瘤坏死因子-α（TNF-α）在小鼠抗原激活的人T细胞中的相互作用。

Interaction of IL-1 beta, IL-6 and tumour necrosis factor-alpha (TNF-alpha) in human T cells activated by murine antigens.

作者信息

Panzer S, Madden M, Matsuki K

机构信息

Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis.

出版信息

Clin Exp Immunol. 1993 Sep;93(3):471-8. doi: 10.1111/j.1365-2249.1993.tb08203.x.

DOI:10.1111/j.1365-2249.1993.tb08203.x
PMID:8370177
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1554907/
Abstract

We used a mixed leucocyte culture between human T cells and irradiated murine splenocytes which allowed us to distinguish between cytokine production from the responder and stimulator cells by the use of species-specific assays for mRNA up-regulation. Using this model of T cell activation by antigen, we studied the effects of human antigen-presenting cell-derived cytokines IL-1 beta, IL-6 and TNF-alpha on the activation of human T cell subsets. We show in this system that exogenously added IL-1 beta, IL-6 and TNF-alpha induces IL-2 receptor (R) up-regulation and IL-2 production, and proliferation by both CD4+ and CD8+ cells. The addition of IL-1 beta induces IL-6 mRNA, and anti-IL-1 antibodies or an IL-1R antagonist protein completely suppresses IL-6 and TNF-alpha supported proliferation. Similarly, addition of IL-6 or TNF-alpha induces up-regulation of IL-1 beta mRNA. However, anti-IL-6 and anti-IL-6R antibodies only partially block proliferation supported by IL-1 beta. These findings suggest that IL-6 and TNF-alpha will induce IL-2R up-regulation/IL-2 secretion via the induction of IL-1 beta production.

摘要

我们采用人T细胞与经照射的鼠脾细胞之间的混合白细胞培养，通过使用针对mRNA上调的种属特异性检测方法，使我们能够区分应答细胞和刺激细胞产生的细胞因子。利用这种抗原激活T细胞的模型，我们研究了人抗原呈递细胞衍生的细胞因子IL-1β、IL-6和TNF-α对人T细胞亚群激活的影响。我们在该系统中表明，外源性添加的IL-1β、IL-6和TNF-α可诱导IL-2受体（R）上调以及IL-2产生，并促进CD4+和CD8+细胞增殖。添加IL-1β可诱导IL-6 mRNA表达，而抗IL-1抗体或IL-1R拮抗剂蛋白可完全抑制IL-6和TNF-α支持的增殖。同样，添加IL-6或TNF-α可诱导IL-1β mRNA上调。然而，抗IL-6和抗IL-6R抗体仅部分阻断IL-1β支持的增殖。这些发现表明，IL-6和TNF-α将通过诱导IL-1β产生来诱导IL-2R上调/IL-2分泌。

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