B细胞
免疫系统
调节性B细胞
多克隆抗体
生物
多克隆B细胞反应
B-1电池
免疫学
细胞生物学
受体
分子生物学
抗体
T细胞
B细胞受体
抗原提呈细胞
遗传学
作者
Shannon E. McGettigan,Lazaro E. Aira,Gaurav Kumar,Romain Ballet,Eugene C. Butcher,Nicole Baumgarth,Gudrun F. Debes
标识
DOI:10.1038/s41467-023-44382-w
摘要
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.
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