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

Sophie Hillion (), Anjelica Miranda, Christelle Dantec, Marina Boudigou, Laëtitia Pottier, Divi Cornec, Raul M. Torres and Roberta Pelanda
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Sophie Hillion: and CHU de Brest
Anjelica Miranda: University of Colorado School of Medicine, Anschutz Medical Campus
Christelle Dantec: Inserm
Marina Boudigou: Inserm
Laëtitia Pottier: Inserm
Divi Cornec: and CHU de Brest
Raul M. Torres: University of Colorado School of Medicine, Anschutz Medical Campus
Roberta Pelanda: University of Colorado School of Medicine, Anschutz Medical Campus

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract 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.

Date: 2024
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DOI: 10.1038/s41467-024-52224-6

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