Abstract
Background: GITR (glucocorticoid-induced TNFR-related protein), a member of the TNF receptor superfamily, is highly expressed on the activated T cells, including CD4+ T cells, CD8+ T cells and Tregs. Upon binding to its ligand, GITR serves as a co-stimulating molecule, playing a vital role in T cell proliferation and anti-tumor activity by converting immunesuppressive Tregs into antitumor effector T cells. Activating GITR by agonistic antibodies, in combination of immune checkpoint inhibitors (ICIs), has been thought to be a highly plausible combo strategy which is now been tested in a few clinical studies. However, we are lacking preclinical models to evaluate efficacy of therapeutic GITR agonistic antibodies, which usually don’t cross-bind to mouse targets. To fill this gap, we developed a human GITR knock-in model (GITR HuGEMM).
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