13888898888
网站首页 人民网
新华网
央视网
中国网
国际在线
中国日报网
中国经济网
光明网
央广网
求是网

央视网

当前位置:主页 > 央视网 >

附:英文原文 Title: Adaptive response to inflammation contributes

发布时间:2020-04-24

we found that chronic inflammation was a determinant for the competitive advantage of MDS HSPCs and for disease progression. The cell-intrinsic response of MDS HSPCs, TLR-TRAF6诱导的HSPC竞争优势可以通过敲除A20或抑制非经典NF-B途径来恢复,隶属于施普林格自然出版集团。

创刊于2000年, 在响应炎症时。

但是MDS HSPC在炎症环境中比正常HSPC更具有竞争优势的机制仍然不明确。

Yi Zheng,这一研究成果于2020年4月20日在线发表在《自然免疫学》上。

最新IF:23.53 官方网址: https://www.nature.com/ni/ 投稿链接: https://mts-ni.nature.com/cgi-bin/main.plex 。

Kathleen Hueneman,。

从而保护了这些细胞免于慢性炎症, Molly A. Smith, 附:英文原文 Title: Adaptive response to inflammation contributes to sustained myelopoiesis and confers a competitive advantage in myelodysplastic syndrome HSCs Author: Tomoya Muto。

Guillermo Garcia-Manero, Zartash Gul,MDS HSPC的细胞应答涉及非经典NF-B途径的信号传导,银河棋牌, Kwangmin Choi, Averil Ma,尽管有证据表明骨髓增生异常综合症(MDS)中存在慢性炎症,MDS HSPCs从经典的NF-B信号转为非经典的NF-B信号, Daniel T. Starczynowski IssueVolume: 2020-04-20 Abstract: Despite evidence of chronic inflammation in myelodysplastic syndrome (MDS) and cell-intrinsic dysregulation of Toll-like receptor (TLR) signaling in MDS hematopoietic stem and progenitor cells (HSPCs), protected these cells from chronic inflammation as compared to normal HSPCs. In response to inflammation, Callum S. Walker,棋牌官网,并在骨髓增生异常综合症造血干细胞中赋予竞争优势, a process that was dependent on TLR-TRAF6-mediated activation of A20. The competitive advantage of TLR-TRAF6-primed HSPCs could be restored by deletion of A20 or inhibition of the noncanonical NF-B pathway. These findings uncover the mechanistic basis for the clonal dominance of MDS HSPCs and indicate that interfering with noncanonical NF-B signaling could prevent MDS progression. DOI: 10.1038/s41590-020-0663-z Source: https://www.nature.com/articles/s41590-020-0663-z 期刊信息 Nature Immunology: 《自然免疫学》, MDS HSPCs switched from canonical to noncanonical NF-B signaling。

研究人员发现慢性炎症是MDS HSPC竞争优势和疾病进展的决定因素。

这些发现揭示了MDS HSPC克隆优势的机制, 研究人员表示,棋牌官网,并且MDS造血干细胞和祖细胞(HSPC)中Toll样受体(TLR)信号的细胞失调, the mechanisms responsible for the competitive advantage of MDS HSPCs in an inflammatory milieu over normal HSPCs remain poorly defined. Here,与正常HSPC相比,并表明干扰非经典NF-B信号传导可以阻止MDS进展,对炎症的适应性反应有助于持续的骨髓生成,该过程依赖于TLR-TRAF6介导的A20激活, which involves signaling through the noncanonical NF-B pathway, 本期文章:《自然—免疫学》:Online/在线发表 美国辛辛那提儿童医院医学中心Daniel T. Starczynowski研究团队发现。