Anti-GITR/Tnfrsf18 Picoband® Antibody Fluoro594 Conjugated

Tumor necrosis factor receptor superfamily member 18 (TNFRSF18) also known as activation-inducible TNFR family receptor (AITR) or glucocorticoid-induced TNFR-related protein (GITR) is a protein that in humans is encoded by the TNFRSF18 gene. It is mapped to 4; 4 E2. This gene encodes a member of the TNF-receptor superfamily. The encoded receptor has been shown to have increased expression upon T-cell activation, and it is thought to play a key role in dominant immunological self-tolerance maintained by CD25 (+) CD4 (+) regulatory T cells. Knockout studies in mice also suggest the role of this receptor is in the regulation of CD3-driven T-cell activation and programmed cell death. Three alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.

Receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway.

1. Grohmann, U., Volpi, C., Fallarino, F., Bozza, S., Bianchi, R., Vacca, C., Orabona, C., Belladonna, M. L., Ayroldi, E., Nocentini, G., Boon, L., Bistoni, F., Fioretti, M. C., Romani, L., Riccardi, C., Puccetti, P. Reverse signaling through GITR ligand enables dexamethasone to activate IDO in allergy. Nature Med. 13: 579-586, 2007. 2. Gurney, A. L., Marsters, S. A., Huang, A., Pitti, R. M., Mark, M., Baldwin, D. T., Gray, A. M., Dowd, P., Brush, J., Heldens, S., Schow, P., Goddard, A. D., Wood, W. I., Baker, K. P., Godowski, P. J., Ashkenazi, A. Identification of a new member of the tumor necrosis factor family and its receptor, a human ortholog of mouse GITR. Curr. Biol. 9: 215-218, 1999. 3. Ji, H., Liao, G., Faubion, W. A., Abadia-Molina, A. C., Cozzo, C., Laroux, F. S., Caton, A., Terhorst, C. Cutting edge: the natural ligand for glucocorticoid-induced TNF receptor-related protein abrogates regulatory T cell suppression. J. Immun. 172: 5823-5827, 2004.