GITR – GITRL Pathway

Glucocorticoid-induced TNFR-related protein (GITR; CD357; TNFRSF18) is an activating receptor on the surface of T cells and other immune cells, binding to its ligand GITRL (TNFSF18). Once exposure to tumor antigen activates a T cell, the number of GITR receptors on its surface increases. On the activated T cell, GITR acts as a co-stimulatory receptor, meaning that it is a receptor whose signaling enhances cell reproduction and the generation of cancer-killing activity. Activation of GITR signaling can also help to enhance immunity through the activation of cytotoxic T cells and inhibition of Treg activity. The GITR/GITRL pathway can shift the immune balance toward anti-tumor immunity by strengthening effector T cell responses and weakening tumor-protective regulatory networks but also play a dual role in autoimmunity. While its activation can help control tumor growth, excessive stimulation may promote autoreactive T cell activity, aggravating autoimmune inflammation. 

LIT:  Modulation of GITR for cancer immunotherapy: D.A. Schaer, et al.; Curr. Opin. Immunol. 24, 217 (2012) • Rationale for anti-GITR cancer immunotherapy: D.A. Knee, et al.; Eur. J. Cancer 67, 1 (2016) • New emerging targets in cancer immunotherapy: the role of GITR: G. Buzzatti, et al.; ESMO Open 4, e000738 (2020) • The Role of GITR/GITRL Interaction in Autoimmune Diseases: J. Tian, et al.; Front. Immunol. 11, 588682 (2020)

Biologically Active GITR and GITRL Proteins  

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