Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Int Immunopharmacol. 2020 Mar;80:106221. doi: 10.1016/j.intimp.2020.106221. Epub 2020 Jan 30.
CD28 and CTLA-4 are both important stimulatory receptors for the regulation of T cell activation. Because receptors share common ligands, B7.1 and B7.2, the expression and biological function of CTLA-4 is important for the negative regulation of T cell responses. Therefore, elimination of CTLA-4 can result in the breakdown of immune tolerance and the development of several diseases such as autoimmunity. Inhibitory signals of CTLA-4 suppress T cell responses and protect against autoimmune diseases in many ways. In this review, we summarize the structure, expression and signaling pathway of CTLA-4. We also highlight how CTLA-4 defends against potentially self-reactive T cells. Finally, we discuss how the CTLA-4 regulates a number of autoimmune diseases that indicate manipulation of this inhibitory molecule is a promise as a strategy for the immunotherapy of autoimmune diseases.
CD28 和 CTLA-4 都是调节 T 细胞激活的重要刺激受体。由于受体共享共同的配体 B7.1 和 B7.2，CTLA-4 的表达和生物学功能对于 T 细胞反应的负调节非常重要。因此，消除 CTLA-4 可能导致免疫耐受的破坏和自身免疫等多种疾病的发生。CTLA-4 的抑制信号通过多种方式抑制 T 细胞反应并预防自身免疫性疾病。在这篇综述中，我们总结了 CTLA-4 的结构、表达和信号通路。我们还强调了 CTLA-4 如何抵御潜在的自身反应性 T 细胞。最后，我们讨论了 CTLA-4 如何调节多种自身免疫性疾病，这表明对这种抑制分子的调控可能成为治疗自身免疫性疾病的一种策略。
