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These results suggest that therapeutically targeting GITR represents a unique approach to cancer immunotherapy and suggests that a multimeric fusion protein may provide increased agonistic potential versus an antibody
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These findings support further study into combination partners for GITRL-FP that may augment CD8 T-cell priming as well as provide hypotheses that can be tested in human clinical trials exploring GITR agonists including GITRL-FP.
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Expression of human GITR was comparable with that of mouse GITR in tumor-infiltrating Tregs despite being drastically lower in other human TILs and in many human peripheral blood populations.
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anti-GITR mAb shifts Treg populations to enable immune attack on tumors, with clinical implications for molecular markers to modify emerging treatments.
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Continuous GITR stimulation through B cell Gitrl acts protective in a mouse model of atherosclerosis by regulating the balance between regulatory and effector memory CD4(+) T cells.
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these results indicate that blockade of GITR signaling can ameliorate arthritis progression mainly by modulating the follicular helper T cell response
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GITR appears as a potential target for intervention during infection by the parasite Toxoplasma gondii, even though further studies are still necessary to better characterize the immune response triggered by GITR activation during T. gondii infection
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our data suggest a critical role for GITR in Treg cell homeostasis and indicate that Ptpn22 independently affects the differentiation status of Treg cells and their homeostatic behavior
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These findings provide further support for the continued development of agonist anti-GITR antibodies as an immunotherapeutic strategy for osteosarcoma. We suggest that our proposed immunotherapy could be developed further to improve osteosarcoma treatment
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Th9 cells and iTregs are developmentally linked and GITR can subvert tolerogenic conditions to boost Th9 immunity.
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GITR is a crucial player in differentiation of thymic regulatory T cells and expansion of regulatory T cells, including both thymic regulatory T cells and peripheral regulatory T cells.
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enhanced GITR-triggering mediates its protective, anti-viral effect on the CD8 T cell compartment by boosting CD4 T cell help.
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A CD4 T cell-intrinsic role for GITR in sustaining early CD8 and late humoral responses to collectively promote control of chronic LCMV clone 13 infection.
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GITRL expressed on macrophages drives cytokine release and T cell activation, resulting in neuropathic pain via GITR-dependent actions. The GITRL-GITR pathway might represent a novel target for the treatment of neuropathic pain.
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Data show that GITR agonist antibody alters Treg lineage stability inducing an inflammatory effector T cell phenotype. The resultant loss of lineage stability causes Treg to lose their intra-tumor immune suppressive function.
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Gene expression in the Gitr locus is regulated by NF-kappaB and Foxp3 through an enhancer.
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Inhibition of GITR decreases leukocyte cell adhesion.
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The effects of GITR activation on Treg cells can have different outcomes depending on the experimental context ranging from expansion in normal mice to death in the Inflammatory bowel disease model.
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GITR triggering on CD4(+)T cells increases poststroke inflammation and decreases the number of neural stem/progenitor cells induced by ischemia (iNSPCs).
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these data suggest that GITR plays a role in the survival of CD8 memory phenotype T cells
