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Safety Data Sheet (SDS) FITC Anti-mouse GITR Antibody     Product Data Sheet (PDF)    
FITC Anti-mouse GITR Antibody
1231540 200 µg $270.00       
Clone: DTA-1
Isotype: Rat IgG2b, λ
Reactivity: Mouse
Immunogen: Mouse CD25+ CD4+ T cells
Formulation: Phosphate-buffered solution, pH 7.2, containing 0.09% sodium azide.
Preparation: The antibody was purified by affinity chromatography, and conjugated with FITC under optimal conditions. The solution is free of unconjugated FITC.
Concentration: 0.5 mg/ml
Storage & Handling: The antibody solution should be stored undiluted between 2°C and 8°C, and protected from prolonged exposure to light. Do not freeze.

FC - Quality tested

Recommended Usage:

Each lot of this antibody is quality control tested by immunofluorescent staining with flow cytometric analysis. For flow cytometric staining, the suggested use of this reagent is ≤1.0 µg per million cells in 100 µl volume. It is recommended that the reagent be titrated for optimal performance for each application.

Application References:

1. De Luca A, et al. 2007. J. Immunol. 179:5999. PubMed

C57BL/6 splenocytes were stained with

C57BL/6 splenocytes were stained with DTA-1 FITC.


GITR (glucocorticoid-induced TNFR-related gene) is a member of the TNF receptor superfamily, also known as TNFRSF18 and AITR (in humans). It is expressed at low levels on resting T lymphocytes and at high levels on CD25+ CD4+ Tregs. The expression of GITR on T cells can be upregulated upon activation. Interaction of GITR with its ligand (GITRL) has been demonstrated to augment T cell activation, proliferation, cytokine production as well as MAPKs and NF-κB activation, and abrogate the inhibitory function of CD25+ CD4+ Tregs. In vivo activation of GITR causes development of autoimmune diseases and restores the suppressed immune response.

Other Names: Glucocorticoid-induced TNFR -related gene, TNFRSF18
Structure: 66-70 kD homodimer of TNFR superfamily member.
Distribution: Low levels on resting T cells, B cells, and macrophages; high levels on CD25+ CD4+ Tregs and CD25+ CD4+ CD8- thymocytes.
Function: Stimulation of GITR can abrogate or reduce the inhibitory function of CD25+ CD4+ Treg cells. In vivo activation of GITR may lead to the development of autoimmune diseases.
Ligand Receptor: GITR ligand (GITRL).
Regulation: Activation of T and B cells can upregulate GITR expression.
Antigen References:

1. Tone M, et al. 2003. Proc. Natl. Acad. Sci. USA 100:15059.
2. Shimizu J, et al. 2002 Nat. Immunol. 3:135.
3. Stephens GL, et al. 2004. J. Immunol. 173:5008.
4. McHugh RS, et al. 2002. Immunity 16:311.