Secreted IgM modulates IL-10 expression in B cells
Shannon Eileen McGettigan,
Lazaro Emilio Aira,
Gaurav Kumar,
Romain Ballet,
Eugene C. Butcher,
Nicole Baumgarth and
Gudrun F. Debes ()
Additional contact information
Shannon Eileen McGettigan: Thomas Jefferson University
Lazaro Emilio Aira: Thomas Jefferson University
Gaurav Kumar: Thomas Jefferson University
Romain Ballet: Veterans Affairs Palo Alto Health Care System
Eugene C. Butcher: Veterans Affairs Palo Alto Health Care System
Nicole Baumgarth: University of California Davis
Gudrun F. Debes: Thomas Jefferson University
Nature Communications, 2024, vol. 15, issue 1, 1-12
Abstract:
Abstract IL-10+ B cells are critical for immune homeostasis and restraining immune responses in infection, cancer, and inflammation; however, the signals that govern IL-10+ B cell differentiation are ill-defined. Here we find that IL-10+ B cells expand in mice lacking secreted IgM ((s)IgM–/–) up to 10-fold relative to wildtype (WT) among all major B cell and regulatory B cell subsets. The IL-10+ B cell increase is polyclonal and presents within 24 hours of birth. In WT mice, sIgM is produced prenatally and limits the expansion of IL-10+ B cells. Lack of the high affinity receptor for sIgM, FcμR, in B cells translates into an intermediate IL-10+ B cell phenotype relative to WT or sIgM–/– mice. Our study thus shows that sIgM regulates IL-10 programming in B cells in part via B cell-expressed FcμR, thereby revealing a function of sIgM in regulating immune homeostasis.
Date: 2024
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-023-44382-w
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DOI: 10.1038/s41467-023-44382-w
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