E3 ubiquitin ligases and their control of T cell autoreactivity.

E3 ubiquitin ligases and their control of T cell autoreactivity.
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E3泛素连接酶及其对T细胞自身反应性的控制。

DOI:
10.1186/ar1842
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发表时间:
2005
影响因子:
4.9
通讯作者:
Mueller, DL
Mueller, DL
中科院分区:
医学2区
文献类型:
--
作者:
Bonnevier, JL;Zhang, R;Mueller, DL

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T 细胞耐受性的丧失是大多数自身免疫性疾病发生的基础。然而,潜在自身反应性 T 细胞失活所涉及的分子机制的不确定性阻碍了重新建立免疫耐受的治疗策略的设计。最近,E3 泛素连接酶已被证明可以介导 T 细胞持久无反应状态(称为克隆无能)的发展。在这篇综述中,我们将讨论 E3 连接酶控制 T 细胞激活和防止自身免疫发展的机制。
A loss of T cell tolerance underlies the development of most autoimmune diseases. The design of therapeutic strategies to reinstitute immune tolerance, however, is hampered by uncertainty regarding the molecular mechanisms involved in the inactivation of potentially autoreactive T cells. Recently, E3 ubiquitin ligases have been shown to mediate the development of a durable state of unresponsiveness in T cells called clonal anergy. In this review, we will discuss the mechanisms used by E3 ligases to control the activation of T cells and prevent the development of autoimmunity.
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