FLT3L-dependent dendritic cells control tumor immunity by modulating Treg and NK cell homeostasis.

CTLA-4 Flt3-L Foxp3(+) regulatory T cells PD-1 TARGET TCGA Zbtb46 dendritic cells effector T cells natural killer cells transcriptome tumor microenvironment

Journal

Cell reports. Medicine
ISSN: 2666-3791
Titre abrégé: Cell Rep Med
Pays: United States
ID NLM: 101766894

Informations de publication

Date de publication:
19 Dec 2023
Historique:
received: 22 03 2022
revised: 05 06 2023
accepted: 02 10 2023
medline: 21 12 2023
pubmed: 21 12 2023
entrez: 20 12 2023
Statut: ppublish

Résumé

FLT3-L-dependent classical dendritic cells (cDCs) recruit anti-tumor and tumor-protecting lymphocytes. We evaluate cancer growth in mice with low, normal, or high levels of cDCs. Paradoxically, both low or high numbers of cDCs improve survival in mice with melanoma. In low cDC context, tumors are restrained by the adaptive immune system through influx of effector T cells and depletion of Tregs and NK cells. High cDC numbers favor the innate anti-tumor response, with massive recruitment of activated NK cells, despite high Treg infiltration. Anti CTLA-4 but not anti PD-1 therapy synergizes with FLT3-L therapy in the cDC

Identifiants

pubmed: 38118422
pii: S2666-3791(23)00433-0
doi: 10.1016/j.xcrm.2023.101256
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

101256

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

Auteurs

Paul Régnier (P)

Institut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Sorbonne Université, INSERM, UMR_S959, Immunology-Immunopathology-Immunotherapy, Paris, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Department of Internal Medicine and Clinical Immunology, DMU3ID, Paris, France.

Mathias Vetillard (M)

Université de Paris Cité, Centre for Inflammation Research, INSERM U1149, CNRS ERL8252, Paris, France; Dendritic Cells and Adaptive Immunity Unit, Institut Pasteur, Paris, France.

Adèle Bansard (A)

Institut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Université Paris Cité, Faculté de Médecine, Paris, France.

Eméranne Pierre (E)

Université Paris Cité, Faculté de Médecine, Paris, France.

Xinyue Li (X)

Sorbonne Université, INSERM, UMR_S959, Immunology-Immunopathology-Immunotherapy, Paris, France.

Nicolas Cagnard (N)

Structure Fédérative de Recherche Necker, Université Paris Descartes, Paris, France.

Emmanuel L Gautier (EL)

Inserm, UMR_S1166, Sorbonne Université, Hôpital Pitié-Salpêtrière, Paris, France.

Pierre Guermonprez (P)

Université de Paris Cité, Centre for Inflammation Research, INSERM U1149, CNRS ERL8252, Paris, France; Dendritic Cells and Adaptive Immunity Unit, Institut Pasteur, Paris, France.

Bénédicte Manoury (B)

Institut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France.

Katrina Podsypanina (K)

Institut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Institut Curie, PSL Research University, CNRS, Sorbonne Université, UMR3664, Paris, France.

Guillaume Darrasse-Jèze (G)

Institut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Sorbonne Université, INSERM, UMR_S959, Immunology-Immunopathology-Immunotherapy, Paris, France; Université Paris Cité, Faculté de Médecine, Paris, France. Electronic address: guillaume.darrasse-jeze@inserm.fr.

Classifications MeSH