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E3 ubiquitin ligase Cbl-b suppresses proallergic T cell development and allergic airway inflammation.E3 泛素连接酶 Cbl-b 抑制变应性 T 细胞的发育和过敏性气道炎症。
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The ubiquitin ligase Stub1 negatively modulates regulatory T cell suppressive activity by promoting degradation of the transcription factor Foxp3.泛素连接酶 Stub1 通过促进转录因子 Foxp3 的降解来负调控调节性 T 细胞的抑制活性。
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Stabilization of the transcription factor Foxp3 by the deubiquitinase USP7 increases Treg-cell-suppressive capacity.去泛素化酶 USP7 通过稳定转录因子 Foxp3 增加 Treg 细胞抑制能力。
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T cell activation threshold regulated by E3 ubiquitin ligase Cbl-b determines fate of inducible regulatory T cells.E3 泛素连接酶 Cbl-b 调控 T 细胞活化阈值决定诱导性调节性 T 细胞的命运。
J Immunol. 2013 Jul 15;191(2):632-9. doi: 10.4049/jimmunol.1202068. Epub 2013 Jun 7.
6
E3 ubiquitin ligase Cbl-b regulates Pten via Nedd4 in T cells independently of its ubiquitin ligase activity.E3 泛素连接酶 Cbl-b 通过 Nedd4 在 T 细胞中调节 Pten，而不依赖其泛素连接酶活性。
Cell Rep. 2012 May 31;1(5):472-82. doi: 10.1016/j.celrep.2012.04.008.
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Program death-1 regulates peripheral T cell tolerance via an anergy-independent mechanism.程序性细胞死亡蛋白-1 通过一种非无能机制调节外周 T 细胞耐受。
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Control of T(H)17/T(reg) balance by hypoxia-inducible factor 1.缺氧诱导因子 1 对 T(H)17/T(reg) 平衡的调控。
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In vivo expansion of T reg cells with IL-2-mAb complexes: induction of resistance to EAE and long-term acceptance of islet allografts without immunosuppression.利用白细胞介素-2-单克隆抗体复合物在体内扩增调节性T细胞：诱导对实验性自身免疫性脑脊髓炎的抗性以及在无免疫抑制情况下对胰岛同种异体移植物的长期接受。
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T-cell receptor-induced NF-kappaB activation is negatively regulated by E3 ubiquitin ligase Cbl-b.T细胞受体诱导的核因子κB激活受到E3泛素连接酶Cbl-b的负调控。
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E3泛素连接酶Cbl-b通过靶向Foxp3进行泛素化来调节胸腺来源的CD4+CD25+调节性T细胞的发育。

E3 Ubiquitin Ligase Cbl-b Regulates Thymic-Derived CD4+CD25+ Regulatory T Cell Development by Targeting Foxp3 for Ubiquitination.

作者信息

Zhao Yixia, Guo Hui, Qiao Guilin, Zucker Mark, Langdon Wallace Y, Zhang Jian

机构信息

Department of Microbial Infection and Immunity, The Ohio State University, Columbus, OH 43210;

Department of Microbial Infection and Immunity, The Ohio State University, Columbus, OH 43210; Section of Nephrology, Department of Medicine, University of Chicago, Chicago, IL 60637; and.

出版信息

J Immunol. 2015 Feb 15;194(4):1639-45. doi: 10.4049/jimmunol.1402434. Epub 2015 Jan 5.

DOI:10.4049/jimmunol.1402434
PMID:25560411
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4324371/
Abstract

CD28 costimulation is essential for the development of thymic-derived CD4(+)CD25(+)Foxp3(+) regulatory T cells ("tTregs"). E3 ubiquitin ligase Cbl-b has been shown to regulate CD28 dependence of T cell activation. In this paper, we report that the loss of Cbl-b partially but significantly rescues the defective development of tTregs in Cd28(-/-) mice. This partial rescue is independent of IL-2. Mechanistically, Cbl-b binds to Foxp3 upon TCR stimulation and, together with Stub1, targets Foxp3 for ubiquitination and subsequently degradation in the proteasome. As Cbl-b self-ubiquitination and proteasomal degradation is impaired in Cd28(-/-) T cells, the defective development of tTregs in Cd28(-/-) mice may in part be due to increased Foxp3 ubiquitination and degradation targeted by Stub1 and Cbl-b. Treating Cd28(-/-) mice with a proteasome inhibitor completely rescues defective tTreg development in these mice. Therefore, Cbl-b, together with Stub1, ubiquitinate Foxp3, and regulate tTreg development.

摘要

CD28共刺激对于胸腺来源的CD4(+)CD25(+)Foxp3(+)调节性T细胞（“tTregs”）的发育至关重要。E3泛素连接酶Cbl-b已被证明可调节T细胞活化对CD28的依赖性。在本文中，我们报告Cbl-b的缺失部分但显著地挽救了Cd28(-/-)小鼠中tTregs的缺陷发育。这种部分挽救与白细胞介素-2无关。从机制上讲，Cbl-b在TCR刺激后与Foxp3结合，并与Stub1一起将Foxp3靶向泛素化，随后在蛋白酶体中降解。由于Cd28(-/-)T细胞中Cbl-b的自身泛素化和蛋白酶体降解受损，Cd28(-/-)小鼠中tTregs的缺陷发育可能部分归因于Stub1和Cbl-b靶向的Foxp3泛素化和降解增加。用蛋白酶体抑制剂治疗Cd28(-/-)小鼠可完全挽救这些小鼠中缺陷性tTreg的发育。因此，Cbl-b与Stub1一起使Foxp3泛素化，并调节tTreg的发育。