FOXO1 and FOXO3 Cooperatively Regulate Innate Lymphoid Cell Development.
FOXO
IL-15
development
innate lymphocyte cells (ILCs)
natural killer cells
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2022
2022
Historique:
received:
13
01
2022
accepted:
19
04
2022
entrez:
27
6
2022
pubmed:
28
6
2022
medline:
29
6
2022
Statut:
epublish
Résumé
Natural killer (NK) cells play roles in viral clearance and early surveillance against malignant transformation, yet our knowledge of the underlying mechanisms controlling their development and functions remain incomplete. To reveal cell fate-determining pathways in NK cell progenitors (NKP), we utilized an unbiased approach and generated comprehensive gene expression profiles of NK cell progenitors. We found that the NK cell program was gradually established in the CLP to preNKP and preNKP to rNKP transitions. In line with FOXO1 and FOXO3 being co-expressed through the NK developmental trajectory, the loss of both perturbed the establishment of the NK cell program and caused stalling in both NK cell development and maturation. In addition, we found that the combined loss of FOXO1 and FOXO3 caused specific changes to the composition of the non-cytotoxic innate lymphoid cell (ILC) subsets in bone marrow, spleen, and thymus. By combining transcriptome and chromatin profiling, we revealed that FOXO TFs ensure proper NK cell development at various lineage-commitment stages through orchestrating distinct molecular mechanisms. Combined FOXO1 and FOXO3 deficiency in common and innate lymphoid cell progenitors resulted in reduced expression of genes associated with NK cell development including ETS-1 and their downstream target genes. Lastly, we found that FOXO1 and FOXO3 controlled the survival of committed NK cells
Identifiants
pubmed: 35757763
doi: 10.3389/fimmu.2022.854312
pmc: PMC9218573
doi:
Substances chimiques
Forkhead Box Protein O1
0
Forkhead Box Protein O3
0
FoxO3 protein, mouse
0
Foxo1 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
854312Informations de copyright
Copyright © 2022 Luu, Søndergaard, Peña-Pérez, Kharazi, Krstic, Meinke, Schmied, Frengen, Heshmati, Kierczak, Bouderlique, Wagner, Gustafsson, Chambers, Achour, Kutter, Höglund, Månsson and Kadri.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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