Anti-CTLA-4 antibodies drive myeloid activation and reprogram the tumor microenvironment through FcγR engagement and type I interferon signaling.
Journal
Nature cancer
ISSN: 2662-1347
Titre abrégé: Nat Cancer
Pays: England
ID NLM: 101761119
Informations de publication
Date de publication:
11 2022
11 2022
Historique:
received:
11
10
2021
accepted:
20
09
2022
pubmed:
28
10
2022
medline:
30
11
2022
entrez:
27
10
2022
Statut:
ppublish
Résumé
Despite the clinical success of checkpoint inhibitors, a substantial gap still exists in our understanding of their mechanism of action. While antibodies to cytotoxic T lymphocyte-associated protein-4 (CTLA-4) were developed to block inhibitory signals in T cells, several recent studies have demonstrated that Fcγ receptor (FcγR)-dependent depletion of regulatory T cells (T
Identifiants
pubmed: 36302895
doi: 10.1038/s43018-022-00447-1
pii: 10.1038/s43018-022-00447-1
doi:
Substances chimiques
Receptors, IgG
0
Interferon Type I
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1336-1350Subventions
Organisme : Howard Hughes Medical Institute
Pays : United States
Organisme : Cancer Research UK
ID : C36463/A22246
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C36463/A20764
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C416/A18088
Pays : United Kingdom
Organisme : Cancer Research UK
ID : C33499/A20265
Pays : United Kingdom
Commentaires et corrections
Type : ErratumIn
Informations de copyright
© 2022. The Author(s), under exclusive licence to Springer Nature America, Inc.
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