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Loss of NKG2D in murine NK cells leads to increased perforin production upon long-term stimulation with IL-2.
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-02-12 , DOI: 10.1002/eji.201948222
Daniela Prinz 1 , Klara Klein 1 , Julia List 1 , Vanessa M Knab 1 , Ingeborg Menzl 1 , Nicoletta Leidenfrost 1 , Gerwin Heller 2 , Bojan Polić 3 , Eva Maria Putz 4 , Agnieszka Witalisz-Siepracka 1 , Veronika Sexl 1 , Dagmar Gotthardt 1
Affiliation  

NK cells are innate lymphocytes responsible for lysis of pathogen‐infected and transformed cells. One of the major activating receptors required for target cell recognition is the NK group 2D (NKG2D) receptor. Numerous reports show the necessity of NKG2D for effective tumor immune surveillance. Further studies identified NKG2D as a key element allowing tumor immune escape. We here use a mouse model with restricted deletion of NKG2D in mature NKp46+ cells (NKG2DΔNK). NKG2DΔNK NK cells develop normally, have an unaltered IFN‐γ production but kill tumor cell lines expressing NKG2D ligands (NKG2DLs) less efficiently. However, upon long‐term stimulation with IL‐2, NKG2D‐deficient NK cells show increased levels of the lytic molecule perforin. Thus, our findings demonstrate a dual function of NKG2D for NK cell cytotoxicity; while NKG2D is a crucial trigger for cytotoxicity of tumor cells expressing activating ligands it is also capable to limit perforin production in IL‐2 activated NK cells.

中文翻译:

小鼠 NK 细胞中 NKG2D 的损失导致在用 IL-2 长期刺激后增加穿孔素的产生。

NK 细胞是先天淋巴细胞,负责裂解病原体感染和转化的细胞。靶细胞识别所需的主要激活受体之一是 NK 组 2D (NKG2D) 受体。大量报告显示 NKG2D 对有效的肿瘤免疫监视的必要性。进一步的研究确定 NKG2D 是允许肿瘤免疫逃逸的关键因素。我们在这里使用在成熟 NKp46 +细胞 (NKG2D ΔNK ) 中限制性删除 NKG2D 的小鼠模型。NKG2D ΔNKNK 细胞发育正常,产生的 IFN-γ 未改变,但杀死表达 NKG2D 配体 (NKG2DLs) 的肿瘤细胞系的效率较低。然而,在长期使用 IL-2 刺激后,缺乏 NKG2D 的 NK 细胞表现出溶解分子穿孔素水平升高。因此,我们的研究结果证明了 NKG2D 对 NK 细胞的细胞毒性具有双重功能。虽然 NKG2D 是表达激活配体的肿瘤细胞细胞毒性的关键触发因素,但它也能够限制 IL-2 激活的 NK 细胞中穿孔素的产生。
更新日期:2020-02-12
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