GITRL Antibodies

Target Information

The tumor necrosis factor (TNF) and TNF receptor (TNFR) gene superfamilies regulate numerous biological functions including cell proliferation, differentiation, and survival through regulating the activation of the transcription factor NF-kappa-B and various mitogen-activated protein kinases. The glucocorticoid-induced tumor necrosis factor receptor (GITR) is an emerging member of this family that is expressed on CD4+ CD25+ regulatory T cells and appears to have crucial immune regulation functions. Its ligand GITRL is expressed in endothelial and antigen-presenting cells and can activate NF-kappa-B, induce both pro- and anti-apoptotic effects, inhibit the suppressive activity of regulatory T cells, and co-stimulate responder T cells through GITR. Dominant negative forms of NIK and TRAF2 expressed in transfected 293 cells substantially inhibited NF-kappa-B activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.

Synonyms

Activation-inducible TNF-related ligand; AITR ligand; AITRL; GITR ligand; GITRL; GITRLigand; Glucocorticoid-induced TNF-related ligand; glucocorticoid-induced TNFR-related protein ligand; glucocorticoid-induced-tumor necrosis factor receptor ligand; hGITRL; RP1-15D23.1; TL6; TNF superfamily member 18; Tnfsf18; TNLG2A; tumor necrosis factor (ligand) superfamily member 18; tumor necrosis factor (ligand) superfamily, member 18; tumor necrosis factor ligand 2A; Tumor necrosis factor ligand superfamily member 18; tumor necrosis factor superfamily member 18; UNQ149/PRO175