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人类浆细胞样前体树突状细胞通过糖皮质激素诱导的肿瘤坏死因子受体配体(GITRL)激活自然杀伤细胞。

Human plasmacytoid predendritic cells activate NK cells through glucocorticoid-induced tumor necrosis factor receptor-ligand (GITRL).

作者信息

Hanabuchi Shino, Watanabe Norihiko, Wang Yi-Hong, Wang Yui-Hsi, Ito Tomoki, Shaw Joanne, Cao Wei, Qin F Xiao-Feng, Liu Yong-Jun

机构信息

Department of Immunology and Center for Cancer Immunology Research, The University of Texas M. D. Anderson Cancer Center, 7455 Fannin, Unit 910, Houston, 77030-1903, USA.

出版信息

Blood. 2006 May 1;107(9):3617-23. doi: 10.1182/blood-2005-08-3419. Epub 2006 Jan 5.

Abstract

Plasmacytoid dendritic cell precursors (pDCs) are professional type I interferon-producing cells, a critical cell type in regulating innate and adaptive immune responses. By microarray gene expression analysis, we found that pDCs activated by virus or CpG-ODN preferentially express the ligand for the glucocorticoid-induced tumor necrosis factor receptor (GITRL), which was confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry analysis. Using the same approaches, we found GITR is expressed by activated natural killer (NK) cells and T cells. We show that pDCs activated by CpG-ODN promote NK cell cytotoxicity and interferon (IFN)-gamma production through type I IFNs and GITRL. Using a GITRL-transfected cell line, we further demonstrate that GITRL promotes NK cell cytotoxicity and IFN-gamma production in synergy with interleukin-2 (IL-2), IFN-alpha, and NKG2D triggering. We also demonstrated that pDCs localized in close contact to NK cells in T-cell areas of the tonsils, and a subpopulation of the pDCs expressed GITRL. This study reveals a novel function of GITR/GITRL in pDC-mediated coactivation of NK cells.

摘要

浆细胞样树突状细胞前体(pDCs)是产生I型干扰素的专职细胞,是调节固有免疫和适应性免疫反应的关键细胞类型。通过微阵列基因表达分析,我们发现病毒或CpG-ODN激活的pDCs优先表达糖皮质激素诱导的肿瘤坏死因子受体(GITRL)的配体,这一点通过逆转录聚合酶链反应(RT-PCR)和流式细胞术分析得到了证实。使用相同的方法,我们发现活化的自然杀伤(NK)细胞和T细胞表达GITR。我们发现,CpG-ODN激活的pDCs通过I型干扰素和GITRL促进NK细胞的细胞毒性和干扰素(IFN)-γ的产生。使用转染了GITRL的细胞系,我们进一步证明GITRL与白细胞介素-2(IL-2)、IFN-α和NKG2D触发协同作用,促进NK细胞的细胞毒性和IFN-γ的产生。我们还证明,pDCs定位于扁桃体T细胞区与NK细胞紧密接触的位置,并且一部分pDCs表达GITRL。这项研究揭示了GITR/GITRL在pDC介导的NK细胞共激活中的新功能。

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