Target intelligence / Profile preview

Glucocorticoid-Induced Tumor Necrosis Factor Receptor (GITR)

Target
GITR
Molecular classification
Receptor, Tumor Necrosis Factor Receptor Superfamily (TNFRSF)
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Overview

GITR (Glucocorticoid-Induced Tumor Necrosis Factor Receptor), also known as TNFRSF18, CD357, or AITR, is a type I transmembrane protein and a member of the TNF receptor superfamily. It is constitutively expressed on regulatory T cells and upregulated on activated T cells. GITR interacts with its ligand GITRL, primarily expressed on antigen-presenting cells. GITR signaling plays a complex role in regulating immune responses, acting as a co-stimulatory signal for effector T cells, modulating the suppressive function of regulatory T cells, and regulating NK cell activity. It is implicated in cancer immunity, autoimmunity, inflammation, and cardiovascular disease.

Other names
TNFRSF18CD357AITR (Activation-Inducible TNFR Family Receptor)
02

Mechanism of action

GITR engagement provides co-stimulatory signals, modulates regulatory T cell suppression, and/or regulates NK cell activity depending on the cell type and context.

03

Biological functions

T cell co-stimulationRegulatory T cell modulationNK cell regulationImmune responseCell proliferationApoptosisCytokine production
04

Disease associations

CancerAutoimmunityInflammationCardiovascular disease
05

Safety considerations

Modulation of immune responses in autoimmune diseases requires careful consideration due to the potential for exacerbating disease or causing other immune-related adverse effects.In cancer therapy, balancing stimulation of anti-tumor immunity with the potential for immune-related adverse events is a key challenge.

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