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Transcription factors Foxo3a and Foxo1 couple the E3 ligase Cbl-b to the induction of Foxp3 expression in induced regulatory T cells.转录因子 Foxo3a 和 Foxo1 将 E3 连接酶 Cbl-b 与诱导调节性 T 细胞中 Foxp3 表达的诱导相偶联。
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调节外周免疫反应以控制器官特异性自身免疫的机制。

Mechanisms that regulate peripheral immune responses to control organ-specific autoimmunity.

作者信息

Hoyne Gerard F

机构信息

School of Health Sciences, University of Notre Dame Australia, 19 Mouat Street, Fremantle, WA 6959, Australia.

出版信息

Clin Dev Immunol. 2011;2011:294968. doi: 10.1155/2011/294968. Epub 2011 Apr 28.

DOI:10.1155/2011/294968
PMID:21603204
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3095406/
Abstract

The immune system must balance the need to maintain a diverse repertoire of lymphocytes to be able to fight infection with the need to maintain tolerance to self-proteins. The immune system places strict regulation over the ability of T cells to produce the major T cell growth factor interleukin 2 as this cytokine can influence a variety of immune outcomes. T cells require the delivery of two signals, one through the antigen receptor and a second through the costimulatory receptor CD28. The immune system uses a variety of E3 ubiquitin ligases to target signaling proteins that function downstream of the TCR and CD28 receptors. Mutations in these E3 ligases can lead to a breakdown in immune tolerance and development of autoimmunity. This paper will examine the role of a range of E3 ubiquitin ligases and signaling pathways that influence the development of T-cell effector responses and the development of organ-specific autoimmune diseases such as type 1 diabetes.

摘要

免疫系统必须在维持多样化的淋巴细胞库以对抗感染的需求与维持对自身蛋白质耐受性的需求之间取得平衡。免疫系统对T细胞产生主要T细胞生长因子白细胞介素2的能力进行严格调控,因为这种细胞因子会影响多种免疫结果。T细胞需要传递两种信号,一种通过抗原受体,另一种通过共刺激受体CD28。免疫系统利用多种E3泛素连接酶来靶向在TCR和CD28受体下游起作用的信号蛋白。这些E3连接酶的突变会导致免疫耐受性的破坏和自身免疫性疾病的发生。本文将探讨一系列E3泛素连接酶和信号通路在影响T细胞效应反应发展以及1型糖尿病等器官特异性自身免疫性疾病发展中的作用。