Preparation and Storage
Background: GITR/TNFRSF18
GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a transmembrane TNF receptor superfamily member that functions in immune regulation. GITR is expressed on CD4+CD25+ regulatory T cells (Treg) as well as on subsets of thymocytes, lymph node cells, and splenocytes, and it is upregulated on antigen-activated conventional CD4+ and CD8+ T cells. GITR binding by GITR Ligand/TNFSF18 costimulates the proliferation and activation of CD4+ or CD8+ conventional T cells. It also induces the proliferation of Treg but inhibits the ability of Treg to suppress immune responses. This can result in the development of autoimmunity, increased tumor cell killing by effector T cells, and increased inflammation in arthritis, allergic asthma, and inflammatory bowel disease. GITR is also expressed on sympathetic neurons where it enhances NGF-induced neurite outgrowth and branching.
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Long Name:
Glucocorticoid Induced TNF Receptor Family Related Gene
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Entrez Gene IDs:
8784 (Human); 21936 (Mouse); 500598 (Rat); 102146362 (Cynomolgus Monkey)
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Alternate Names:
Activation-inducible TNFR family receptor; AITR; AITRTNF receptor superfamily activation-inducible protein; CD357 antigen; CD357; GITR; GITR-D; GITRtumor necrosis factor receptor superfamily member 18; Glucocorticoid-induced TNFR-related protein; TNFRSF18; tumor necrosis factor receptor superfamily, member 18