Optimization of the Irf8 +32-kb enhancer disrupts dendritic cell lineage segregation.


Journal

Nature immunology
ISSN: 1529-2916
Titre abrégé: Nat Immunol
Pays: United States
ID NLM: 100941354

Informations de publication

Date de publication:
07 Oct 2024
Historique:
received: 01 02 2024
accepted: 09 09 2024
medline: 8 10 2024
pubmed: 8 10 2024
entrez: 7 10 2024
Statut: aheadofprint

Résumé

Autoactivation of lineage-determining transcription factors mediates bistable expression, generating distinct cell phenotypes essential for complex body plans. Classical type 1 dendritic cell (cDC1) and type 2 dendritic cell (cDC2) subsets provide nonredundant functions for defense against distinct immune challenges. Interferon regulatory factor 8 (IRF8), the cDC1 lineage-determining transcription factor, undergoes autoactivation in cDC1 progenitors to establish cDC1 identity, yet its expression is downregulated during cDC2 differentiation by an unknown mechanism. This study reveals that the Irf8 +32-kb enhancer, responsible for IRF8 autoactivation, is naturally suboptimized with low-affinity IRF8 binding sites. Introducing multiple high-affinity IRF8 sites into the Irf8 +32-kb enhancer causes a gain-of-function effect, leading to erroneous IRF8 autoactivation in specified cDC2 progenitors, redirecting them toward cDC1 and a novel hybrid DC subset with mixed-lineage phenotypes. Further, this also causes a loss-of-function effect, reducing Irf8 expression in cDC1s. These developmental alterations critically impair both cDC1-dependent and cDC2-dependent arms of immunity. Collectively, our findings underscore the significance of enhancer suboptimization in the developmental segregation of cDCs required for normal immune function.

Identifiants

pubmed: 39375550
doi: 10.1038/s41590-024-01976-w
pii: 10.1038/s41590-024-01976-w
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
ID : R01AI150297
Organisme : U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
ID : R21AI164142
Organisme : U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
ID : R01AI162643
Organisme : U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
ID : R21AI163421
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : R01CA248919

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.

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Auteurs

Feiya Ou (F)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Tian-Tian Liu (TT)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Pritesh Desai (P)

Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Stephen T Ferris (ST)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.

Sunkyung Kim (S)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Haolin Shen (H)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA, USA.

Ray A Ohara (RA)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Suin Jo (S)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Jing Chen (J)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

J Luke Postoak (JL)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Siling Du (S)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Michael S Diamond (MS)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Department of Medicine, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Department of Molecular Microbiology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
The Andrew M. and Jane M. Bursky Center for Human Immunology and Immunotherapy Programs, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Theresa L Murphy (TL)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.

Kenneth M Murphy (KM)

Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. kmurphy@wustl.edu.

Classifications MeSH