Anti-GITRL TNFSF18 Antibody

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. 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-κB, 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-κB activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.

Cytokine that binds to TNFRSF18/AITR/GITR. Regulates T- cell responses. Can function as costimulator and lower the threshold for T-cell activation and T-cell proliferation. Important for interactions between activated T-lymphocytes and endothelial cells. Mediates activation of NF-kappa-B. Triggers increased phosphorylation of STAT1 and up-regulates expression of VCAM1 and ICAM1 (PubMed:23892569) . Promotes leukocyte adhesion to endothelial cells (PubMed:23892569) . Regulates migration of monocytes from the splenic reservoir to sites of inflammation (By similarity) .

GITRL antibody can be stored at 4°C for three months and -20°C, stable for up to one year. Avoid repeated freeze-thaw cycles. Antibodies should not be exposed to prolonged high temperatures.