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Target intelligence / Profile preview
Glucocorticoid-Induced Tumor Necrosis Factor Receptor-Related Protein (GITR)
- Target
- GITR
- Molecular classification
- Receptor, Type I transmembrane protein, Tumor necrosis factor receptor superfamily (TNFRSF)
01
Overview
Glucocorticoid-Induced Tumor Necrosis Factor Receptor-Related Protein (GITR), also known as TNFRSF18, CD357, or AITR, is a type I transmembrane protein belonging to the tumor necrosis factor receptor superfamily (TNFRSF). It is constitutively expressed at high levels on CD25+CD4+ regulatory T cells (Tregs) and upregulated on all T cell subsets upon activation. GITR acts as a co-stimulatory surface receptor for T cell activation, promoting proliferation and cytokine production. Its ligand, GITRL, is mainly expressed by activated antigen-presenting cells. GITR plays a complex role in immune regulation, impacting both effector and regulatory T cell functions, as well as NK cell activity. Agonistic antibodies targeting GITR are being explored as cancer immunotherapy agents.
- Other names
- TNFRSF18CD357AITR (Activation-Inducible TNFR Family Receptor)
02
Mechanism of action
Agonistic antibodies enhance antitumor immunity by promoting effector cytotoxicity and modulating immunosuppressive elements within the tumor microenvironment.
03
Biological functions
Immune responseT cell activationT cell proliferationCytokine productionTreg function modulationApoptosis regulationNK cell regulation
04
Disease associations
CancerAutoimmunityChronic InflammationInfection
05
Safety considerations
Aberrant costimulation through AITR/GITRL axis may be involved in autoimmune pathogenesis.Overexpression/activity has been linked to unstable plaque formation/atherosclerosis progression experimentally.
06
Interacting drugs
Agonistic antibodies targeting GITR
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