Details zur Publikation
|DOI / URL||Link|
|Titel (primär)||Maternal B cell signaling orchestrates fetal development in mice|
|Autor||Busse, M.; Langwisch, S.; Tedford, K.; Fischer, K.-D.; Zenclussen, A.C.|
|Journal / Serie||Development|
|Topic||T9 Healthy Planet|
|Keywords||B cells; MyD88; high frequency ultrasound; pre-term birth; pregnancy|
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.
|Busse, M., Langwisch, S., Tedford, K., Fischer, K.-D., Zenclussen, A.C. (2022):
Maternal B cell signaling orchestrates fetal development in mice
Development 149 (8), dev.199783