| First Author | McGettigan SE | Year | 2024 |
| Journal | Nat Commun | Volume | 15 |
| Issue | 1 | Pages | 324 |
| PubMed ID | 38182585 | Mgi Jnum | J:351182 |
| Mgi Id | MGI:7575173 | Doi | 10.1038/s41467-023-44382-w |
| Citation | McGettigan SE, et al. (2024) Secreted IgM modulates IL-10 expression in B cells. Nat Commun 15(1):324 |
| abstractText | 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, FcmuR, 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 FcmuR, thereby revealing a function of sIgM in regulating immune homeostasis. |
