YTHDF2 suppresses the plasmablast genetic program and promotes germinal center formation.

B cells CP: Immunology YTHDF antibodies epigenetics germinal center m6A mRNA plasma cells post-transcriptional

Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
03 05 2022
Historique:
received: 21 12 2021
revised: 25 02 2022
accepted: 12 04 2022
entrez: 4 5 2022
pubmed: 5 5 2022
medline: 7 5 2022
Statut: ppublish

Résumé

Antibody-mediated immunity is initiated by B cell differentiation into multiple cell subsets, including plasmablast, memory, and germinal center (GC) cells. B cell differentiation trajectories are determined by transcription factors, yet very few mechanisms that specifically determine early B cell fates have been described. Here, we report a post-transcriptional mechanism that suppresses the plasmablast genetic program and promotes GC B cell fate commitment. Single-cell RNA-sequencing analysis reveals that antigen-specific B cell precursors at the pre-GC stage upregulate YTHDF2, which enhances the decay of methylated transcripts. Ythdf2-deficient B cells exhibit intact proliferation and activation, whereas differentiation into GC B cells is blocked. Mechanistically, B cells require YTHDF2 to attenuate the plasmablast genetic program during GC seeding, and transcripts of key plasmablast-regulating genes are methylated and bound by YTHDF2. Collectively, this study reveals how post-transcriptional suppression of gene expression directs appropriate B cell fate commitment during initiation of the adaptive immune response.

Identifiants

pubmed: 35508130
pii: S2211-1247(22)00542-3
doi: 10.1016/j.celrep.2022.110778
pmc: PMC9108551
pii:
doi:

Substances chimiques

Transcription Factors 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

110778

Informations de copyright

Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

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Auteurs

Amalie Grenov (A)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Hadas Hezroni (H)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Lior Lasman (L)

Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.

Jacob H Hanna (JH)

Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.

Ziv Shulman (Z)

Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel. Electronic address: ziv.shulman@weizmann.ac.il.

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Classifications MeSH