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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >An update on cell intrinsic negative regulators of the NLRP3 inflammasome
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An update on cell intrinsic negative regulators of the NLRP3 inflammasome

机译:NLRP3炎性小体细胞内在负调节剂的更新

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Inflammasomes are multimeric protein complexes that promote inflammation (through specific cleavage and production of bioactive IL‐1β and IL‐18) and pyroptotic cell death. The central role of inflammasomes in combating infection and maintaining homeostasis has been studied extensively. Although inflammasome‐mediated inflammation and cell death are vital to limit pathogenic insults and to promote wound healing/tissue regeneration, unchecked/uncontrolled inflammation, and cell death can cause cytokine storm, tissue damage, autoinflammatory and autoimmune diseases, and even death in the afflicted individuals. NLRP3 is one of the major cytosolic sensors that assemble an inflammasome. Given the adverse consequences of uncontrolled inflammasome activation, our immune system has developed tiered mechanisms to inhibit NLRP3 inflammasome activation. In this review, we highlight and discuss recent advances and our current understanding of mechanisms by which NLRP3 inflammasome can be negatively regulated.
机译:炎症小体是多聚体蛋白复合物,可促进炎症(通过特异性裂解和生物活性IL-1β和IL-18的产生)和焦细胞凋亡。炎症小体在抵抗感染和维持体内平衡方面的核心作用已得到广泛研究。尽管炎性体介导的炎症和细胞死亡对于限制病原体侵袭和促进伤口愈合/组织再生至关重要,但是不受控制的炎症/不受控制的炎症以及细胞死亡可能导致细胞因子风暴,组织损伤,自体炎症和自身免疫性疾病,甚至折磨受难者个人。 NLRP3是组装炎症小体的主要胞质传感器之一。鉴于不受控制的炎性体激活的不利后果,我们的免疫系统已开发出抑制NLRP3炎性体激活的分层机制。在这篇综述中,我们重点介绍并讨论了最新进展以及我们对NLRP3炎性小体可以被负调控的机制的当前理解。

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