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GITR Inhibitor

Chemicals Research

Updated on May 30, 2019

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An Overview of GITR

Glucocorticoid-induced tumor necrosis factor receptor (GITR) is the 18th member of the tumor necrosis factor receptor superfamily (TNFRSF) and is a surface molecule of CD4+CD25+ regulatory T cell (Treg) from thoracic gland. GITR belongs to members of TNFRSF with CD40, CD27 and OX40. Its intracellular region is homologous with these members, and extracellular domain is rich in cysteine motifs. GITR is a homologous dimer transmembrane glycoprotein of 70kD, mainly expressed on resting Treg cells in thymus and peripheral lymphoid organs, and a little on CD4+CD25+ T cells, macrophages and dendritic cells, and its ligand is GITRL. GITR/GITRL has many important biological activities, including cell proliferation, differentiation and survival.

Agonist of GITR

Many immune molecules can be used as agonists of GITR to promote the expression of GITR in multiple steps, such as IL2, lipopolysaccharide. The expression of GITR on CD4+CD25+T cells, CD8+T cells and macrophages in peripheral lymphoid organs was low, and the expression of GITR was increased after stimulation of CD4+ and CD8+T cells with anti CD3 antibody and IL-2. The expression of GITR in B cells and macrophages increased slightly after stimulation with lipopolysaccharide or IFN-γ. It can be seen that GITR is mainly expressed in CD4+CD25+ cells of thymus and peripheral lymphoid organs, but the expression of other types of cells is increased after activation, although the expression of other types of cells is low.
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