Glucocorticoid-induced TNF receptor (GITR) (GITR)

Glucocorticoid-induced TNF receptor (GITR), also known as TNFRSF18 or TR11, is a member of the tumor necrosis factor receptor superfamily that plays a critical role in regulating immune responses. It is constitutively expressed at high levels on regulatory T cells (Tregs) and is upregulated on activated effector T cells (Teffs) and natural killer (NK) cells. Activation of GITR by its ligand (GITRL) or agonistic antibodies provides co-stimulatory signals that enhance Teff proliferation and cytokine production while potentially inhibiting or depleting Tregs, thereby promoting anti-tumor immunity. In oncology, GITR is a prominent target for immunotherapy, with several agonistic monoclonal antibodies in clinical development, often in combination with PD-1/PD-L1 inhibitors. Beyond cancer, GITR signaling is involved in the pathogenesis of autoimmune and inflammatory diseases, making it a versatile target for modulating the immune system. Note: In some biotechnology contexts, particularly within argenx, 'TRLL' may refer to 'Therapeutic Regional Learning Liaisons,' which are professional roles rather than biological targets; however, 'TR11' (often rendered as 'TRLL' in OCR) is the established synonym for the GITR receptor.

Other names

TNFRSF18TR11AITRCD357Glucocorticoid-induced TNFR-related proteinTumor necrosis factor receptor superfamily member 18

Agonism of GITR to co-stimulate effector T cells and deplete regulatory T cells (Tregs)