Suppr超能文献

前沿:CD4+CD25+调节性细胞的接触介导抑制涉及一种颗粒酶B依赖性、穿孔素非依赖性机制。

Cutting edge: contact-mediated suppression by CD4+CD25+ regulatory cells involves a granzyme B-dependent, perforin-independent mechanism.

作者信息

Gondek David C, Lu Li-Fan, Quezada Sergio A, Sakaguchi Shimon, Noelle Randolph J

机构信息

Department of Microbiology and Immunology, Dartmouth Medical School and Norris Cotton Cancer Center, Lebanon, NH 03756, USA.

出版信息

J Immunol. 2005 Feb 15;174(4):1783-6. doi: 10.4049/jimmunol.174.4.1783.

Abstract

CD4+CD25+ regulatory T cells (Treg) are potent immunosuppressive cells that are pivotal in the regulation of peripheral tolerance. In this report, we identify granzyme B (GZ-B) as one of the key components of Treg-mediated suppression. Induction of regulatory activity is correlated with the up-regulation of GZ-B expression. Proof of a functional involvement of GZ-B in contact-mediated suppression by Treg is shown by the reduced ability of Treg from GZ-B-/- mice to suppress as efficiently as Treg from WT mice. GZ-B-mediated suppression is perforin independent, because suppression by Treg from perforin-/- and WT is indistinguishable. Additionally, suppression mediated by Treg appears to be mediated, in part, by the induction of apoptosis in the CD4+CD25- effector cell. In summary, GZ-B is one of the key mechanisms through which CD4+CD25+ Treg induce cell contact-mediated suppression.

摘要

CD4+CD25+调节性T细胞(Treg)是强大的免疫抑制细胞,在调节外周免疫耐受中起关键作用。在本报告中,我们确定颗粒酶B(GZ-B)是Treg介导的抑制作用的关键组成部分之一。调节活性的诱导与GZ-B表达的上调相关。GZ-B-/-小鼠的Treg抑制能力低于野生型(WT)小鼠,这表明GZ-B在Treg接触介导的抑制中发挥功能性作用。GZ-B介导的抑制不依赖穿孔素,因为穿孔素-/-和WT小鼠的Treg抑制作用没有差异。此外,Treg介导的抑制似乎部分是通过诱导CD4+CD25-效应细胞凋亡来实现的。总之,GZ-B是CD4+CD25+ Treg诱导细胞接触介导的抑制作用的关键机制之一。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验