糖皮质激素诱导肿瘤坏死因子受体（GITR）/糖皮质激素诱导肿瘤坏死因子受体配体（GITRL）：不仅仅是一种效应性T细胞共刺激系统。

GITR/GITRL: more than an effector T cell co-stimulatory system.

作者信息

Nocentini Giuseppe, Ronchetti Simona, Cuzzocrea Salvatore, Riccardi Carlo

机构信息

Dipartimento di Medicina Clinica e Sperimentale, Sezione di Farmacologia, Tossicologia e Chemioterapia, Università di Perugia, Perugia, Italy.

出版信息

Eur J Immunol. 2007 May;37(5):1165-9. doi: 10.1002/eji.200636933.

DOI:10.1002/eji.200636933

PMID:17407102

Abstract

Glucocorticoid-induced TNFR-related protein (GITR) is a member of the TNFR superfamily, expressed in several cells and tissues including T lymphocytes, NK cells and antigen-presenting cells (APC). GITR activation, upon interaction with its ligand (GITRL), functions as a co-activating signal. GITRL is mainly expressed on APC and GITR/GITRL interaction is important for the development of immune response. This review summarizes recent results about the GITR/GITRL system, focusing on the interplay between APC, effector and regulatory T cells.

摘要

糖皮质激素诱导的肿瘤坏死因子受体相关蛋白（GITR）是肿瘤坏死因子受体超家族的成员，在包括T淋巴细胞、自然杀伤细胞和抗原呈递细胞（APC）在内的多种细胞和组织中表达。GITR与其配体（GITRL）相互作用后被激活，发挥共激活信号的作用。GITRL主要在APC上表达，GITR/GITRL相互作用对免疫反应的发展很重要。本综述总结了关于GITR/GITRL系统的最新研究结果，重点关注APC、效应性T细胞和调节性T细胞之间的相互作用。