Targeting GITR in cancer immunotherapy - there is no perfect knowledge.
cancer
cytotoxic T-lymphocyte Antigen-4 (CTLA-4)
glucocorticoid-induced TNFR-related protein (GITR)
immunotherapy
programmed death-1 (PD-1)
Journal
Oncotarget
ISSN: 1949-2553
Titre abrégé: Oncotarget
Pays: United States
ID NLM: 101532965
Informations de publication
Date de publication:
19 06 2023
19 06 2023
Historique:
medline:
21
6
2023
pubmed:
19
6
2023
entrez:
19
6
2023
Statut:
epublish
Résumé
Glucocorticoid-induced TNFR-related protein (GITR) belongs to the TNFR superfamily (TNFRSF) and stimulates both the acquired and innate immunity. GITR is broadly expressed on immune cells, particularly regulatory T cells (Tregs) and natural killer (NK) cells. Given its potential to promote T effector function and impede Treg immune suppression, GITR is an attractive target for cancer immunotherapy. Preclinically, GITR agonists have demonstrated potent anti-tumor efficacy singly and in combination with a variety of agents, including PD-1 blockade. Multiple GITR agonists have been advanced into the clinic, although the experience with these agents has been disappointing. Recent mechanistic insights into the roles of antibody structure, valency, and Fc functionality in mediating anti-tumor efficacy may explain some of the apparent inconsistency or discordance between preclinical data and observed clinical efficacy.
Identifiants
pubmed: 37335294
pii: 28461
doi: 10.18632/oncotarget.28461
pmc: PMC10278658
doi:
Substances chimiques
Glucocorticoid-Induced TNFR-Related Protein
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
614-621Subventions
Organisme : NCI NIH HHS
ID : R01 CA257265
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA271407
Pays : United States
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