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Glucocorticoid-Induced TNF Receptor-Related Protein (GITR)
- Target
- GITR
- Molecular classification
- Receptor, Type I transmembrane protein, Tumor Necrosis Factor Receptor Superfamily (TNFRSF)
01
Overview
Glucocorticoid-Induced TNF Receptor-Related Protein (GITR), also known as TNFRSF18 or CD357, is a type I transmembrane protein belonging to the tumor necrosis factor receptor superfamily (TNFRSF). It is constitutively expressed at high levels on regulatory T cells (Tregs) and upregulated upon activation in all T cell subsets. GITR interacts with its ligand, GITRL, which is expressed by antigen-presenting cells. GITR functions as a co-stimulatory molecule, enhancing T cell activation, proliferation, and cytokine production. It also plays a regulatory role in modulating the balance between immune activation and suppression, and is targeted for cancer immunotherapy.
- Other names
- TNFRSF18CD357AITR (Activation-Inducible TNFR Family Receptor)
02
Mechanism of action
Agonist anti-GITR antibodies enhance anti-tumor immunity by boosting effector functions while reducing immunosuppression from regulatory populations.
03
Biological functions
Co-stimulatory moleculeEnhances T cell receptor (TCR) signalingPromotes T cell proliferationPromotes cytokine productionModulates immune balanceInhibits regulatory T-cell suppressive activity
04
Disease associations
CancerAutoimmune diseasesInflammationCardiovascular disease/AtherosclerosisViral/parasitic infectionAllergic inflammation
05
Safety considerations
Overactivation can exacerbate autoimmune/inflammatory diseasesPotential for cytokine release syndrome with agonistic antibodies
06
Biomarkers
Expression levels on T cells (especially Tregs) as an indicator of activation or regulatory state
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