Anti-Human GITR

NS0-Derived Recombinant Human GITR Extracellular Domain

This antigen affinity purified polyclonal antibody has been 0.2 µm filtered and lyophilized from modified Dulbecco’s phosphate buffered saline (1X PBS) pH 7.2 – 7.3 containing 5.0% w/v trehalose with no calcium, magnesium, or preservatives present.

Lyophilized

The lyophilized antigen affinity purified polyclonal antibody can be stored desiccated at -20°C to -70°C for twelve months from date of receipt. The reconstituted antibody can be stored for at least four weeks at 2-8°C. For long-term storage of the reconstituted antibody, aseptically aliquot into working volumes and store at -20°C to -70°C in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles. No detectable loss of activity was observed after six months.

Next Day Ambient

IHC (NBF/Par.): This antibody should give satisfactory staining results when used at a concentration of 10 µg/ml. The recommended secondary antibody for IHC is PN:G505. For chromogenic detection with high signal and low background use PN:D100 or PN:K107.
Blocking: Approximately 1 - 2 μg/mL of this antibody will block 50% of the binding of 10 ng/mL of rhGITR Ligand to immobilized rhGITR/Fc chimera (100 μL of a 2 μg/mL solution was coated in each well) in a functional ELISA.
CyTOF-ready: Ready to be labeled using established conjugation methods. No BSA or other carrier proteins that could interfere with conjugation.

Goat Anti-Human Glucocorticoid Induced TNF Receptor (GITR) recognizes Human GITR. This antigen affinity purified polyclonal antibody was purified using a proprietary chromatographic technique that includes covalently immobilizing the antigen proteins or peptides to agarose based beads. This purification method enhances specificity, reduces nonspecific binding of extraneous IgG and provides you with the most reliable reagent available for your early discovery research.

GITR (glucocorticoid-induced tumor necrosis factor receptor) also known as TNFRSF18, is a surface receptor molecule that has been shown to be involved in inhibiting the suppressive activity of T-regulatory cells and extending the survival of T-effector cells.¹ GITR is involved in the regulation of T-cell receptor mediated cell death. Constitutive expression of a transfected GITR gene induces resistance to apoptosis induced by anti CD3 monoclonal antibodies.

GITR ligand interferes with the suppressor activity of CD4(+) CD25(+) regulatory T-cells.²

1. Shimizu, J. et al. (2002) Nature Immunology 3:135–142.
2. Ji, Hb. et al. (2004)Journal of Immunology 172: 5823