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CD39 is a negative regulator of P2X7-mediated inflammatory cell death in mast cells

机译:CD39是肥大细胞中P2X7介导的炎性细胞死亡的负调节剂

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摘要

BackgroundMast cells (MCs) are major contributors to an inflammatory milieu. One of the most potent drivers of inflammation is the cytokine IL-1β, which is produced in the cytoplasm in response to danger signals like LPS. Several controlling mechanisms have been reported which limit the release of IL-1β. Central to this regulation is the NLRP3 inflammasome, activation of which requires a second danger signal with the capacity to subvert the homeostasis of lysosomes and mitochondria. High concentrations of extracellular ATP have the capability to perturb the plasma membrane by activation of P2X7 channels and serve as such a danger signal. In this study we investigate the role of P2X7 channels and the ecto-5´-nucleotidase CD39 in ATP-triggered release of IL-1β from LPS-treated mast cells.
机译:背景肥大细胞(MCs)是导致炎症的主要因素。最有效的炎症驱动因素之一是细胞因子IL-1β,它是在细胞质中响应LPS等危险信号而产生的。已经报道了限制IL-1β释放的几种控制机制。该调节的中心是NLRP3炎性小体,其激活需要第二个危险信号,该信号具有破坏溶酶体和线粒体稳态的能力。高浓度的细胞外ATP具有通过激活P2X7通道扰动质膜的能力,并可以作为这种危险信号。在这项研究中,我们研究了P2X7通道和ecto-5´核苷酸酶CD39在ATP触发的LPS处理的肥大细胞释放IL-1β中的作用。

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