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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Immobilization of rolling NK cells on platelet-borne P-selectin under flow by proinflammatory stimuli, interleukin-12, and leukotriene B4.
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Immobilization of rolling NK cells on platelet-borne P-selectin under flow by proinflammatory stimuli, interleukin-12, and leukotriene B4.

机译：促炎性刺激，白介素12和白三烯B4在流动下将滚动的NK细胞固定在血小板传播的P-选择素上。

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摘要

Recruitment of leukocytes from bloodstream to extrahematic sites is tightly regulated by a variety of adhesion molecules that are expressed on the leukocytes and the vessel walls. In this manuscript, we describe the interactions between natural killer (NK) cells and activated, autologous platelets under physiologic flow. We found that surface-adherent human platelets are capable of recruiting human NK cells from flow and that this recruitment is characterized by an initial tethering followed by a rolling phase. Both phases were dependent on the adhesion molecule P-selectin and its counter-ligand on the NK cells (P-selectin glycoprotein ligand 1). Activation of rolling NK cells with inflammatory mediators commonly found in atherosclerotic plaques (interleukin-12 and leukotriene B4) causes immediate cessation of the rolling process and conversion to stationary adhesion. Blocking antibodies to the adhesion molecules membrane-activated complex-1 and leukocyte function antigen-1 inhibited this conversion. Our data suggest that platelets deposited at sites of vascular injury may provide an alternative substrate to endothelial cells for initial recruitment of NK cells to the vessel wall. This may result in extravasation of the NK cells if the appropriate chemotactic signal is applied. These data implicate the P-selectin and integrin family of adhesion molecules in the recruitment of NK cells to atherosclerotic sites.
机译：白细胞从血流到外流部位的募集受到在白细胞和血管壁上表达的多种粘附分子的严格调控。在这份手稿中，我们描述了自然杀伤（NK）细胞与生理流下活化的自体血小板之间的相互作用。我们发现，表面粘附的人血小板能够从血流中募集人NK细胞，并且这种募集的特征是初始束缚，随后是滚动阶段。这两个阶段均取决于粘附分子P-选择素及其在NK细胞上的反配体（P-选择素糖蛋白配体1）。滚动的NK细胞被动脉粥样硬化斑块（白介素12和白三烯B4）中常见的炎性介质激活，导致滚动过程立即停止并转变为固定粘附。粘附分子膜激活复合物1和白细胞功能抗原1的封闭抗体抑制了这种转化。我们的数据表明，沉积在血管损伤部位的血小板可能为内皮细胞提供了另一种底物，用于将NK细胞最初募集到血管壁。如果施加适当的趋化信号，这可能导致NK细胞外渗。这些数据暗示在NK细胞募集到动脉粥样硬化部位中的粘附分子的P-选择蛋白和整联蛋白家族。

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