In vitro studies using an agonistic anti-GITR monoclonal antibody (mAb; DTA-1) or GITRL transfectants and soluble GITRL have shown that the GITR–GITRL pathway induces positive costimulatory signals leading to the activation of CD4+ and CD8+ effector T cells as well as Treg cells, despite their opposing effector functions. The administration of DTA-1 or soluble GITRL immunoglobulin has been shown to enhance anti-tumour immunity by augmenting CD4+ and/or CD8+ T-cell activation. Collectively, these studies have demonstrated the T-cell costimulatory functions of GITR in vitro and in vivo; however, they have not addressed the direct contribution of endogenous GITRL expressed on antigen-presenting cells.
Drug targets for cancer: GITRL research reagents
Other vital drug targets for cancer likeGITRL:
Piao J, Kamimura Y, Iwai H, et al. Enhancement of T-cell-mediated anti-tumour immunity via the ectopically expressed glucocorticoid-induced tumour necrosis factor receptor-related receptor ligand (GITRL) on tumours. Immunology. 2009;127(4):489-499.