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10.1111/jcmm.13124

http://scihub22266oqcxt.onion/10.1111/jcmm.13124
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suck abstract from ncbi


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pmid28276625
      J+Cell+Mol+Med 2017 ; 21 (9 ): 2046-2054
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  • NKG2D ligand RAE1? induces generation and enhances the inhibitor function of myeloid-derived suppressor cells in mice #MMPMID28276625
  • Qian L ; Liu Y ; Wang S ; Gong W ; Jia X ; Liu L ; Ye F ; Ding J ; Xu Y ; Fu Y ; Tian F
  • J Cell Mol Med 2017[Sep]; 21 (9 ): 2046-2054 PMID28276625 show ga
  • Expression of surface NKG2D ligands on tumour cells, which activates nature killer (NK) cells and CD8(+) T cells, is crucial in antitumour immunity. Some types of tumours have evolved mechanisms to suppress NKG2D-mediated immune cell activation, such as tumour-derived soluble NKG2D ligands or sustained NKG2D ligands produced by tumours down-regulate the expression of NKG2D on NK cells and CD8(+) T cells. Here, we report that surface NKG2D ligand RAE1? on tumour cells induces CD11b(+) Gr-1(+) myeloid-derived suppressor cell (MDSC) via NKG2D in vitro and in vivo. MDSCs induced by RAE1? display a robust induction of IL-10 and arginase, and these MDSCs show greater suppressive activity by inhibiting antigen-non-specific CD8(+) T-cell proliferation. Consistently, upon adoptive transfer, MDSCs induced by RAE1? significantly promote CT26 tumour growth in IL-10- and arginase-dependent manners. RAE1? moves cytokine balance towards Th2 but not Th1 in vivo. Furthermore, RAE1? enhances inhibitory function of CT26-derived MDSCs and promotes IL-4 rather than IFN-? production from CT26-derived MDSCs through NKG2D in vitro. Our study has demonstrated a novel mechanism for NKG2D ligand(+) tumour cells escaping from immunosurveillance by facilitating the proliferation and the inhibitory function of MDSCs.
  • |Animals [MESH]
  • |CD11b Antigen/metabolism [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Proliferation [MESH]
  • |Female [MESH]
  • |Interleukin-10/metabolism [MESH]
  • |Interleukin-4/metabolism [MESH]
  • |Ligands [MESH]
  • |Mice, Inbred BALB C [MESH]
  • |Myeloid-Derived Suppressor Cells/*metabolism [MESH]
  • |NK Cell Lectin-Like Receptor Subfamily K/*metabolism [MESH]
  • |Neoplasms/pathology [MESH]
  • |Nuclear Matrix-Associated Proteins/*metabolism [MESH]


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