B cell participation in early embryo/fetal development and the underlying molecular pathways have not been explored.

To understand whether maternal B cell absence or impaired signaling interferes with placental and fetal growth, we paired CD19-deficient (CD19^−/-) mice, females with B cell-specific MyD88 (BMyD88^−/-) or IL-10 (BIL-10^−/-) deficiency as well as WT and MyD88^−/- controls on C57Bl/6 background with BALB/c males. Pregnancies were followed by ultrasound and Doppler measurements.

Implantation number was reduced in BMyD88^−/- and MyD88^−/- mice. Loss of MyD88 or B cell-specific deletion of MyD88 or IL-10 resulted in decreased implantation areas at gestation days (gd)5, 8 and 10, accompanied by reduced placental thickness, diameter and areas at gd10. Uterine artery resistance was enhanced in BIL-10^−/- dams at gd10. Challenge with 0.4mg LPS/kg BW at gd16 revealed that BMyD88^−/-, BIL-10^−/- and CD19^−/- mothers delivered preterm while controls maintained their pregnancy.

B cell specific MyD88 and IL-10 expression is essential for appropriate in utero development. IL-10+B cells are involved in uterine blood flow regulation during pregnancy. Finally, B cell-specific CD19, MyD88 and IL-10 expression influences susceptibility towards preterm birth.