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HBD-3 induces NK cell activation, IFN-gamma secretion and mDC dependent cytolytic function

机译:HBD-3诱导NK细胞活化,IFN-γ分泌和mDC依赖性溶细胞功能

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We previously showed that human beta defensin-3 (hBD-3) activates mDC via TLR1/2. Here we investigated the effects of hBD-3 on NK cell activation state and effector functions. We observed that hBD-3 activates PBMC to secrete IFN-gamma and kill K562 and HUH hepatoma target cells in an NK dependent fashion, and both TLR1/2 and CCR2 are involved. TLR1, TLR2 and CCR2 were expressed on NK cells, and in purified NK culture experiments we observed hBD-3 to directly act on NK cells, resulting in CD69 upregulation and IFN gamma secretion. We also observed mDC-hBD-3 enhanced NK cytolytic activity and IFNy production. These results implicate hBD-3 in its ability to directly activate NK cells and increase NK cell effector function, as well as promote mDC-dependent NK activity. HBD-3 may therefore act as a mediator of innate cell interactions that result in bridging of innate and adaptive immunity. Published by Elsevier Inc.
机译:我们先前显示,人类β防御素3(hBD-3)通过TLR1 / 2激活mDC。在这里,我们调查了hBD-3对NK细胞激活状态和效应功能的影响。我们观察到,hBD-3激活PBMC以分泌IFN-γ并以NK依赖性方式杀死K562和HUH肝癌靶细胞,并且TLR1 / 2和CCR2均参与其中。 TLR1,TLR2和CCR2在NK细胞上表达,在纯化的NK培养实验中,我们观察到hBD-3直接作用于NK细胞,导致CD69上调和IFNγ分泌。我们还观察到mDC-hBD-3增强了NK的细胞溶解活性和IFNγ的产生。这些结果暗示hBD-3直接激活NK细胞并增加NK细胞效应子功能以及促进依赖mDC的NK活性的能力。因此,HBD-3可以充当先天细胞相互作用的介体,从而导致先天免疫和适应性免疫之间的桥梁。由Elsevier Inc.发布

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