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
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

1336-1350

Subventions

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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Auteurs

Ido Yofe (I)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Tomer Landsberger (T)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Adam Yalin (A)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Isabelle Solomon (I)

Cancer Immunology Unit, Research Department of Haematology, University College London Cancer Institute, London, UK.

Cristobal Costoya (C)

Cancer Immunology Unit, Research Department of Haematology, University College London Cancer Institute, London, UK.

Dafne Franz Demane (DF)

Cancer Immunology Unit, Research Department of Haematology, University College London Cancer Institute, London, UK.

Mansi Shah (M)

Cancer Immunology Unit, Research Department of Haematology, University College London Cancer Institute, London, UK.

Eyal David (E)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Chamutal Borenstein (C)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Oren Barboy (O)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Ignacio Matos (I)

Cancer Immunology Unit, Research Department of Haematology, University College London Cancer Institute, London, UK.

Karl S Peggs (KS)

Cancer Immunology Unit, Research Department of Haematology, University College London Cancer Institute, London, UK.

Sergio A Quezada (SA)

Cancer Immunology Unit, Research Department of Haematology, University College London Cancer Institute, London, UK. s.quezada@ucl.ac.uk.

Ido Amit (I)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel. ido.amit@weizmann.ac.il.

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