GITRL

GITRL (Glucocorticoid-Induced TNF Receptor Ligand), also known as TNFSF18, is a co-stimulatory cytokine and a member of the tumor necrosis factor (TNF) superfamily. It serves as the cognate ligand for the GITR receptor (CD357), which is expressed on various immune cells, including effector T cells and regulatory T cells (Tregs). In therapeutic development, GITRL is typically engineered as a recombinant protein or an Fc-fusion construct to act as a GITR agonist. While primarily investigated in oncology to enhance anti-tumor immunity by activating effector T cells and potentially inhibiting Treg-mediated suppression, recent research highlights its potential in autoimmunity. Specifically, GITRL signaling has been shown to drive the proliferation and expansion of Foxp3+ Tregs, which can help restore immune tolerance and ameliorate conditions such as experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. Various constructs, such as hexameric GITRL fusion proteins, have been evaluated in clinical and preclinical settings to modulate these immune pathways.

Other names

Glucocorticoid-induced tumor necrosis factor receptor-related protein ligandTumor necrosis factor ligand superfamily member 18Activation-inducible TNF-related ligand