Bonnevier Jody L, Zhang Ruan, Mueller Daniel L
Rheumatic and Autoimmune Diseases Division, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN, USA.
Arthritis Res Ther. 2005;7(6):233-42. doi: 10.1186/ar1842. Epub 2005 Oct 12.
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.
T细胞耐受性的丧失是大多数自身免疫性疾病发展的基础。然而，恢复免疫耐受性的治疗策略设计受到阻碍，因为涉及潜在自身反应性T细胞失活的分子机制尚不确定。最近，E3泛素连接酶已被证明可介导T细胞中一种称为克隆无能的持久无反应状态的发展。在这篇综述中，我们将讨论E3连接酶用于控制T细胞活化并预防自身免疫性疾病发展的机制。
