Glucocorticoid-Induced TNF Receptor–Related Protein (GITR)

GITR (Glucocorticoid-Induced TNF Receptor–Related Protein), also known as TNFRSF18 or CD357, is a member of the tumor necrosis factor receptor (TNFR) superfamily. It is a type I transmembrane protein primarily expressed on regulatory T cells (Tregs), activated effector T cells, and natural killer (NK) cells. GITR acts as a costimulatory molecule, modulating both innate and adaptive immunity. Upon ligation by its ligand GITRL or agonistic antibodies, GITR activates MAPK/ERK and NFκB pathways, resulting in increased proliferation of effector T cells, enhanced proinflammatory cytokine production, and resistance to suppression by regulatory mechanisms. Modulation of the GITR/GITRL axis has therapeutic potential for cancer immunotherapy and autoimmune diseases.

Other names

TNFRSF18CD357

GITR agonists bind to GITR, activating MAPK/ERK and NFκB pathways, leading to increased proliferation of effector T cells, enhanced proinflammatory cytokine production, and resistance to suppression by regulatory T cells.