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.
Activation-inducible TNF-related ligand; AITR ligand; AITRL; GITR ligand; GITRL; Glucocorticoid-induced TNF-related ligand; glucocorticoid-induced TNFR-related protein ligand; glucocorticoid-induced-tumor necrosis factor receptor ligand; hGITRL; RP1-15D23.1, AITRL, GITRL, TL6, hGITRL; 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
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