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Mutual activation of natural killer cells and monocytes mediated by NKp80-AICL interaction

机译:NKp80-AICL相互作用介导的自然杀伤细胞和单核细胞的相互激活

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摘要

Receptors encoded by the natural killer (NK) cell gene complex (such as NKG2D) govern the reactivity of NK cells. However, the function and ligand(s) of the NK cell gene complex-encoded human NK cell receptor NKp80 remain elusive. Here we demonstrate that NKp80 binds to the genetically linked 'orphan' receptor AICL, which, like NKp80, is absent from rodents. We defined AICL as a myeloid-specific activating receptor that is upregulated by Toll-like receptor stimulation. AICL-NKp80 interactions promoted NK cell-mediated cytolysis of malignant myeloid cells. In addition, during crosstalk between NK cells and monocytes, NKp80 stimulated the release of proinflammatory cytokines from both cell types. Thus, by specifically bridging NK cells and myeloid cells, NKp80-AICL interactions may contribute to the initiation and maintenance of immune responses at sites of inflammation.
机译:由自然杀伤(NK)细胞基因复合物(例如NKG2D)编码的受体控制NK细胞的反应性。但是,NK细胞基因复合物编码的人NK细胞受体NKp80的功能和配体仍然难以捉摸。在这里,我们证明了NKp80与遗传连接的“孤儿”受体AICL结合,而该动物与NKp80一样,是啮齿动物所不具备的。我们将AICL定义为通过Toll样受体刺激上调的髓样特异性激活受体。 AICL-NKp80相互作用促进了恶性骨髓细胞的NK细胞介导的细胞溶解。此外,在NK细胞与单核细胞之间的串扰期间,NKp80刺激了两种细胞中促炎性细胞因子的释放。因此,通过特异地桥接NK细胞和髓样细胞,NKp80-AICL相互作用可有助于炎症部位的免疫应答的起始和维持。

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