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Secreted IgM modulates IL-10 expression in B cells

Author

Listed:
  • 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
    Stanford University School of Medicine)

  • Eugene C. Butcher

    (Veterans Affairs Palo Alto Health Care System
    Stanford University School of Medicine)

  • Nicole Baumgarth

    (University of California Davis
    Johns Hopkins University)

  • Gudrun F. Debes

    (Thomas Jefferson University
    Thomas Jefferson University)

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.

Suggested Citation

  • Shannon Eileen McGettigan & Lazaro Emilio Aira & Gaurav Kumar & Romain Ballet & Eugene C. Butcher & Nicole Baumgarth & Gudrun F. Debes, 2024. "Secreted IgM modulates IL-10 expression in B cells," Nature Communications, Nature, vol. 15(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-023-44382-w
    DOI: 10.1038/s41467-023-44382-w
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