GITR及其在免疫调节中的作用

GITR and its functions in immune regulation

糖皮质激素诱导的TNFR家族相关受体（GITR），也被称为TNFRSF18、AITR（人类）。静止T细胞低水平表达GITR，而CD4^＋CD25^＋调节性T细胞则呈高水平表达。GITR与其配体（GITRL）结合后会增强T细胞激活、增殖、分泌细胞因子、MAPKs和NF-κB激活效应、抑制CD4^＋CD25^＋Treg细胞的功能，从而加强效应性T细胞的活性，有利于增强抗肿瘤免疫和抗病毒免疫。随着生物学环境的变化，GITR激活Siva或者TRAF，起着促进或诱导凋亡的作用。

Glucocorticoid-induced TNFR-related receptor （GITR） is also known as TNFRSF18 or AITR （human）. GITR is expressed at low levels in resting T lymphocytes and up-regulated in CD4 ^＋ CD25^＋ regulatory T cells （Treg）. The combination of GITR and its ligand （GITRL） will promote the activation, proliferation, and cytokine secretion of T cells, the activation of MAPKs and NF-κB, and the inhibition of CD4 ^＋ CD25 ^＋ Treg cells. This will increase the activation of effector T cells and improve the anti-tumor and antiviral immunity. Depending upon the microenviromnent, GITR can activate Siva to promote apoptosis or TRAF to induce apoptosis.