抗GITR Ligand/TNFSF18抗体(Anti-GITR Ligand/TNFSF18, Goat-Poly, Biotin antibody)

Glucocorticoid-induced TNF receptor superfamily-related protein ligand (GITRL) is a member of the TNF superfamily (TNFSF) and has been designated TNFSF18. Mouse GITRL cDNA encodes a 173 amino acid (aa) residues type II membrane protein with a C-terminal extracellular domain of 131 aa, an N-terminal cytoplasmic domain of 23 aa and a transmembrane domain of 19 aa. It shares approximately 60% aa sequence identity with human GITRL (2). Mouse GITRL is expressed at high levels in macrophages, dendritic cells and B cells. The expression is transiently up-regulated by LPS stimulation. GITRL binds to the type I transmembrane protein GITR/TNFRSF18, which is a member of the TNF receptor superfamily that is predominantly expressed on CD25⁺ regulatory CD4⁺ T cells (Treg). GITR is also expressed on naïve CD4⁺ CD25^- T cells, where its expression is up-regulated after antigen-driven activation (1, 2). Ligation of GITR has been found to induce nuclear factor (NF)-kappa B activation via TNF receptor-associated factor 2. GITRL provides co-stimulatory signals for activated CD4⁺ CD25^- T cells to enhance cell proliferation and augment cytokine production. On CD4⁺ CD25⁺ Treg cells, GITRL also provides co-stimulatory signals to induce proliferation, setting Treg cells in an active/hyperproliferactive state that reverses the suppressive function of Treg cells. GITRL-GITR ligation provides important co-stimulatory signals that play important roles in modulating diverse T cell functions (1-4).

1. Ig-reactive CD4+CD25+ T cells from tolerized (New Zealand Black x New Zealand White)F1 mice suppress in vitro production of antibodies to DNA.
   Authors: La Cava A, Ebling FM, Hahn BH
   J. Immunol., 2004;173(5):3542-8.
   Species: Mouse
   Sample Type: Whole Cells
   Application: Flow