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CD4+ T细胞效应子命运选择与功能中的泛素连接酶和去泛素化酶

Ubiquitin Ligases and Deubiquitinating Enzymes in CD4+ T Cell Effector Fate Choice and Function.

作者信息

Layman Awo A K, Oliver Paula M

机构信息

Medical Scientist Training Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104; and.

Department of Pathology, Children's Hospital of Philadelphia and Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104

出版信息

J Immunol. 2016 May 15;196(10):3975-82. doi: 10.4049/jimmunol.1502660.

Abstract

The human body is exposed to potentially pathogenic microorganisms at barrier sites such as the skin, lungs, and gastrointestinal tract. To mount an effective response against these pathogens, the immune system must recruit the right cells with effector responses that are appropriate for the task at hand. Several types of CD4(+) T cells can be recruited, including Th cells (Th1, Th2, and Th17), T follicular helper cells, and regulatory T cells. These cells help to maintain normal immune homeostasis in the face of constantly changing microbes in the environment. Because these cells differentiate from a common progenitor, the composition of their intracellular milieu of proteins changes to appropriately guide their effector function. One underappreciated process that impacts the levels and functions of effector fate-determining factors is ubiquitylation. This review details our current understanding of how ubiquitylation regulates CD4(+) T cell effector identity and function.

摘要

人体在皮肤、肺部和胃肠道等屏障部位会接触到潜在的致病微生物。为了对这些病原体产生有效的反应,免疫系统必须招募合适的细胞,并产生适合手头任务的效应反应。可以招募几种类型的CD4(+) T细胞,包括Th细胞(Th1、Th2和Th17)、滤泡辅助性T细胞和调节性T细胞。面对环境中不断变化的微生物,这些细胞有助于维持正常的免疫稳态。由于这些细胞都来自共同的祖细胞,其细胞内蛋白质环境的组成会发生变化,以适当地指导它们的效应功能。泛素化是一个未得到充分重视的过程,它会影响效应命运决定因子的水平和功能。本综述详细阐述了我们目前对泛素化如何调节CD4(+) T细胞效应特性和功能的理解。

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本文引用的文献

1
Ubiquitylation as a Rheostat for TCR Signaling: From Targeted Approaches Toward Global Profiling.
Front Immunol. 2015 Dec 16;6:618. doi: 10.3389/fimmu.2015.00618. eCollection 2015.
2
Growth Factor FGF2 Cooperates with Interleukin-17 to Repair Intestinal Epithelial Damage.
Immunity. 2015 Sep 15;43(3):488-501. doi: 10.1016/j.immuni.2015.06.024. Epub 2015 Aug 25.
3
Itch WW Domains Inhibit Its E3 Ubiquitin Ligase Activity by Blocking E2-E3 Ligase Trans-thiolation.
J Biol Chem. 2015 Sep 25;290(39):23875-87. doi: 10.1074/jbc.M115.649269. Epub 2015 Aug 5.
5
Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation.
Nature. 2015 Jul 9;523(7559):221-5. doi: 10.1038/nature14452. Epub 2015 Apr 29.
7
Retinoic acid is essential for Th1 cell lineage stability and prevents transition to a Th17 cell program.
Immunity. 2015 Mar 17;42(3):499-511. doi: 10.1016/j.immuni.2015.02.003. Epub 2015 Mar 10.
8
ICOS coreceptor signaling inactivates the transcription factor FOXO1 to promote Tfh cell differentiation.
Immunity. 2015 Feb 17;42(2):239-251. doi: 10.1016/j.immuni.2015.01.017.
9
The chromatin-modifying enzyme Ezh2 is critical for the maintenance of regulatory T cell identity after activation.
Immunity. 2015 Feb 17;42(2):227-238. doi: 10.1016/j.immuni.2015.01.007. Epub 2015 Feb 10.

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