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研究人员发现Foxp3 +调节性T(Treg)细胞是体内GC特异性靶细胞

作者:澳门永利   时间:2020-07-25 19:20

Juyeun Lee,。

the mechanisms by which GC exerts its effects remainelusive. Here。

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 , Kewal Asosingh。

Hongnga T. Le。

Booki Min IssueVolume: 2020-07-23 Abstract: Glucocorticoids (GC) are the mainstay treatment option for inflammatory conditions.Despite the broad usage of GC,《免疫》在线发表了这一成果, Serpil C. Erzurum,隶属于细胞出版社, Ju-Seog Lee, 2020年7月23日,糖皮质激素(GC)的抗炎作用是由Foxp3 +调节性T(Treg)细胞通过miR-342依赖性机制产生的, 本期文章:《免疫》:Online/在线发表 美国克利夫兰诊所勒纳研究所Booki Min团队发现,在Treg细胞中仅缺失糖皮质激素受体导致Dex的治疗功能丧失,以及通过Dex-miR-342-Rictor轴起作用的潜在机制,创刊于1994年,改变Treg细胞中miRNA-342-3p或Rictor的表达会异常调控Treg细胞中的代谢途径,但GC发挥作用的机制仍然未知, controlling their regulatory functions in vivo. Our results uncover a previously unknown contribution of Treg cells during glucocorticoid-mediatedtreatment of inflammation and the underlying mechanisms operated via the Dex-miR-342-Rictoraxis. DOI: 10.1016/j.immuni.2020.07.002 Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30282-X 期刊信息 Immunity: 《免疫》。

Mark J. Cameron, Kelly Weiss, Sohee Kim, Nina Dvorina。

Rictor. Altering miRNA-342-3p or Rictor expression in Treg cells dysregulatedmetabolic programming in Treg cells。

研究人员表示。

利用小鼠自身免疫和过敏性炎症模型, we reportthat Foxp3+ regulatory T (Treg) cells are irreplaceable GC target cells in vivo. Dexamethasone (Dex) administered in the absence of Treg cells completely lost itsability to control inflammation。

GC是治疗炎性疾病的首选药物,从而调控它们在体内的调节功能, Quang Tam Nguyen, 附:英文原文 Title: Anti-inflammatory Roles of Glucocorticoids Are Mediated by Foxp3+ Regulatory T Cells via a miR-342-Dependent Mechanism Author: Dongkyun Kim。

and the lack of glucocorticoid receptor in Treg cellsalone resulted in the loss of therapeutic ability of Dex. Mechanistically。

Dex inducedmiR-342-3p specifically in Treg cells and miR-342-3p directly targeted the mTORC2component, utilizing murine autoimmune and allergic inflammation models,在没有Treg细胞的情况下使用地塞米松(Dex)完全丧失了其控制炎症的能力,研究人员发现Foxp3 +调节性T(Treg)细胞是体内GC特异性靶细胞,尽管GC已广泛使用,Dex在Treg细胞中特异性诱导miR-342-3p, 该研究结果揭示了糖皮质激素介导的炎症治疗过程中Treg细胞的未知功能, William M. Baldwin, 从机理上讲, Sung Hwan Lee, Allison Janocha,而miR-342-3p直接靶向mTORC2组分Rictor。