GITR Extracellular Domain (human, recombinant)

Glucocorticoid-induced TNFR-related protein (GITR), also known as TNF receptor superfamily member 18 (TNFRS18), is a type I transmembrane glycoprotein and member of the tumor necrosis factor receptor superfamily with roles in acquired and innate immunity.¹ It is composed of an extracellular domain that contains a ligand binding site, a transmembrane domain, and a cytoplasmic domain that facilitates the induction of NF-κB signaling.^1,2 GITR is primarily expressed in immature and mature T cells and natural killer (NK) cells but is also expressed at low levels in mast cells, eosinophils, B cells, macrophages, as well as non-lymphoid tissues, osteoclast precursor cells, keratinocytes, and retinal epithelial cells. Upon binding of its ligand GITRL (Item No. 32018), GITR binds various TNF receptor-associated factors (TRAFs) and induces signaling in a cell type-specific manner.³ GITR protein levels are increased in macrophages and dendritic cells in a mouse model of T. gondii infection, and administration of an agonistic anti-GITR antibody increases pro-inflammatory cytokine production in peritoneal fluid and reduces chronic phase parasite burden in the same model.⁴ Protein levels of GITR are also increased on CD4⁺CD25⁺, CD4⁺CD25^high, and CD4⁺CD25⁺CD127^low/- regulatory T cells isolated from patients with systemic lupus erythematosus (SLE) compared with healthy controls.⁵ Intratumor, but not peripheral, administration of an agonistic anti-GITR antibody increases overall survival in a GL261 murine glioma model.⁶ Cayman's GITR Extracellular Domain (human, recombinant) protein can be used for ELISA. This protein consists of 147 amino acids, has a calculated molecular weight of 16 kDa, and a predicted N-terminus of Gln26 after signal peptide cleavage. By SDS-PAGE, under reducing conditions, the molecular mass of the protein is approximately 27 kDa due to apparent post-translational modifications.

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1. Nocentini, G., and Riccardi, C. GITR: A modulator of immune response and inflammation. Therapeutic Targets of the TNF Superfamily 647, 156-173 (2009).

2. Krausz, L.T., Bianchini, R., Ronchetti, S., et al. GITR-GITRL system, a novel player in shock and inflammation. ScientificWorldJournal 7, 533-566 (2007).

3. Clouthier, D.L., and Watts, T.H. Cell-specific and context-dependent effects of GITR in cancer, autoimmunity, and infection. Cytokine Growth Factor Rev. 25(2), 91-106 (2014).

4. Costa, F.R.C., Mota, C.M., Santiago, F.M., et al. GITR activation positively regulates immune responses against Toxoplasma gondii. PLoS One 11(3), e0152622 (2016).

5. Sun, J., Yu, N., Li, X., et al. Aberrant GITR expression on different T cell subsets and the regulation by glucocorticoid in systemic lupus erythematosus. Int. J. Rheum. Dis. 19(2), 199-204 (2016).

6. Miska, J., Rashidi, A., Chang, A.L., et al. Anti-GITR therapy promotes immunity against malignant glioma in a murine model. Cancer Immunol. Immunother. 65(12), 1555-1567 (2016).