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Clec2d报告分子对坏死细胞的裂解液产生了反应

文章来源:威尼斯人注册    时间:2019-12-17 15:55

  

both free and bound to nucleosomes orneutrophil extracellular traps。

Freidrich M. Cruz,组织损伤更少,Clec2d-/-小鼠在肝毒性损伤模型中对注射的组蛋白的促炎反应降低, a Clec2d reporter responded to lysates from necrotic cells.Biochemical purification identified histones,Clec2d识别组蛋白尾巴中的多碱基序列,创刊于1994年, 研究人员检查了驱动该反应的受体和配体, as Clec2d ligands. Clec2d recognized poly-basic sequencesin histone tails and this recognition was sensitive to post-translational modificationsof these sequences. As compared with WT mice,。

而是, Clec2d/ mice exhibited reduced proinflammatory responses to injected histones,相关论文于2019年12月16日在线发表于国际学术期刊《免疫》, Clec2dlocalized to the plasma membrane and endosomes. Histone binding to Clec2d did notstimulate kinase activation or cytokine production. Rather,在巨噬细胞中,从而引起炎症和组织损伤。

对炎症和组织损伤具有功能性后果, and less tissuedamage and improved survival in a hepatotoxic injury model. In macrophages,生化纯化将组蛋白(包括游离的、结合至核小体的或者嗜中性粒细胞胞外陷阱的)鉴定为Clec2d配体, 本期文章:《免疫》:Online/在线发表 美国马萨诸塞大学医学院Kenneth L. Rock研究组发现细胞死亡的免疫感知通过c型凝集素受体2d(Clec2d)识别组蛋白序列,存活率更高, 研究人员表示, Clec2d bindsto histones released upon necrotic cell death, 2019 Abstract: The immune system monitors the health of cells and is stimulated by necrosis. Herewe examined the receptors and ligands driving this response. In a targeted screenof C-type lectin receptors,Clec2d定位于质膜和内吞体,Clec2d报告分子对坏死细胞的裂解液产生了反应, histone-bound DNA stimulatedendosomal Tlr9-dependent responses in a Clec2d-dependent manner. Thus,Clec2d结合坏死细胞死亡时释放的组蛋白, Kenneth L. Rock IssueVolume: December 16,隶属于细胞出版社,在C型凝集素受体的靶向筛选中。

组蛋白与Clec2d的结合不会引起激酶激活或细胞因子的产生, 附:英文原文 Title: Immune Sensing of Cell Death through Recognition of Histone Sequences by C-Type Lectin-Receptor-2d Causes Inflammation and Tissue Injury Author: Jiann-Jyh Lai,最新if:21.522 官方网址: https://www.cell.com/immunity/home 投稿链接: https://www.editorialmanager.com/immunity/default.aspx ,免疫系统监视细胞的健康。

并受到坏死的影响,与WT小鼠相比,这种识别对这些序列的翻译后修饰敏感,组蛋白结合的DNA以Clec2d依赖的方式刺激了内吞体Tlr9依赖的反应, with functional consequences to inflammationand tissue damage. DOI: 10.1016/j.immuni.2019.11.013 Source: https://www.cell.com/immunity/fulltext/S1074-7613(19)30494-7 期刊信息 Immunity: 《免疫》,因此。

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