Document Type
Article
Publication Date
1-5-2024
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.
Recommended Citation
McGettigan, Shannon; Aira, Lazaro; Kumar, Gaurav; Ballet, Romain; Butcher, Eugene; Baumgarth, Nicole; and Debes, Gudrun, "Secreted IgM Modulates IL-10 Expression in B Cells" (2024). Department of Microbiology and Immunology Faculty Papers. Paper 181.
https://jdc.jefferson.edu/mifp/181
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
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Description of Additional Supplementary Files.pdf (91 kB)
Supplementary Data 1.xlsx (1686 kB)
Reporting Summary.pdf (83 kB)
Source Data.xlsx (72 kB)
PubMed ID
38182585
Language
English
Comments
This article is the author's final published version in Nature Communications, Volume 15, Issue 1, 2024, Article number 324.
The published version is available at https://doi.org/10.1038/s41467-023-44382-w.
Copyright © The Author(s) 2024