Maf expression in B cells restricts reactive plasmablast and germinal center B cell expansion.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
12 Sep 2024
Historique:
received: 18 09 2023
accepted: 29 08 2024
medline: 13 9 2024
pubmed: 13 9 2024
entrez: 12 9 2024
Statut: epublish

Résumé

Precise regulation of B cell differentiation is essential for an effective adaptive immune response. Here, we show that B cell development in mice with B cell-specific Maf deletion is unaffected, but marginal zone B cells, germinal centre B cells, and plasmablasts are significantly more frequent in the spleen of naive Maf-deficient mice compared to wild type controls. In the context of a T cell-dependent immunization, Maf deletion causes increased proliferation of germinal centre B cells and extrafollicular plasmablasts. This is accompanied by higher production of antigen-specific IgG1 antibodies with minimal modification of early memory B cells, but a reduction in plasma cell numbers. Single-cell RNA sequencing shows upregulation of genes associated with DNA replication and cell cycle progression, confirming the role of Maf in cell proliferation. Subsequent pathway analysis reveals that Maf influences cellular metabolism, transporter activity, and mitochondrial proteins, which have been implicated in controlling the germinal centre reaction. In summary, our findings demonstrate that Maf acts intrinsically in B cells as a negative regulator of late B cell differentiation, plasmablast proliferation and germinal centre B cell formation.

Identifiants

pubmed: 39266537
doi: 10.1038/s41467-024-52224-6
pii: 10.1038/s41467-024-52224-6
doi:

Substances chimiques

Proto-Oncogene Proteins c-maf 0
Maf protein, mouse 0
Immunoglobulin G 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

7982

Informations de copyright

© 2024. The Author(s).

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Auteurs

Sophie Hillion (S)

LBAI, UMR1227, Univ Brest, Inserm, and CHU de Brest, Brest, France. sophie.hillion@univ-brest.fr.
Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, 80045, USA. sophie.hillion@univ-brest.fr.

Anjelica Miranda (A)

Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, 80045, USA.

Christelle Le Dantec (C)

LBAI, UMR1227, Univ Brest, Inserm, Brest, France.

Marina Boudigou (M)

LBAI, UMR1227, Univ Brest, Inserm, Brest, France.

Laëtitia Le Pottier (L)

LBAI, UMR1227, Univ Brest, Inserm, Brest, France.

Divi Cornec (D)

LBAI, UMR1227, Univ Brest, Inserm, and CHU de Brest, Brest, France.

Raul M Torres (RM)

Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, 80045, USA.

Roberta Pelanda (R)

Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO, 80045, USA.

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