Anti-Human GITRL (G620-GRP)

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-κB and various mitogen-activated protein kinases (reviewed in 1). 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.2,3 Its ligand GITRL is expressed in endothelial and antigen-presenting cells4 and can activate NF-κB, induce both pro- and anti-apoptotic effects, inhibit the suppressive activity of regulatory T cells, and co-stimulate responder T cells through GITR.5 Dominant negative forms of NIK and TRAF2 expressed in transfected 293 cells substantially inhibited NF-κB activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.4