B cell class switch recombination is regulated by DYRK1A through MSH6 phosphorylation.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
16 03 2023
16 03 2023
Historique:
received:
21
06
2022
accepted:
06
03
2023
entrez:
17
3
2023
pubmed:
18
3
2023
medline:
21
3
2023
Statut:
epublish
Résumé
Protection from viral infections depends on immunoglobulin isotype switching, which endows antibodies with effector functions. Here, we find that the protein kinase DYRK1A is essential for B cell-mediated protection from viral infection and effective vaccination through regulation of class switch recombination (CSR). Dyrk1a-deficient B cells are impaired in CSR activity in vivo and in vitro. Phosphoproteomic screens and kinase-activity assays identify MSH6, a DNA mismatch repair protein, as a direct substrate for DYRK1A, and deletion of a single phosphorylation site impaired CSR. After CSR and germinal center (GC) seeding, DYRK1A is required for attenuation of B cell proliferation. These findings demonstrate DYRK1A-mediated biological mechanisms of B cell immune responses that may be used for therapeutic manipulation in antibody-mediated autoimmunity.
Identifiants
pubmed: 36927854
doi: 10.1038/s41467-023-37205-5
pii: 10.1038/s41467-023-37205-5
pmc: PMC10020581
doi:
Substances chimiques
DNA-Binding Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1462Informations de copyright
© 2023. The Author(s).
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