Description:
B cells and in particular IL-10-secreting B cells emerge as important players in immunebalance during pregnancy. We have recently revealed that CD19-deficient (CD19−/−), B cell-specificIL-10-deficient (BIL-10−/−) and B cell-deficient µMT pregnant mice are highly susceptible to LPSinduced preterm birth (PTB). We aimed to analyze the ability of IL-10-secreting cells to protect fromPTB and the underlying mechanisms. Wild type (WT), CD19−/−, BIL-10−/− and µMT mice weretreated with LPS at gd16 and the cellular immune response was investigated 24 h later. LPS-treatedBIL-10−/− dams showed a more pronounced PTB phenotype compared to WT, CD19−/− and µMTfemales, and increased inflammatory and reduced anti-inflammatory mediator concentrations inthe peritoneal cavity and serum. CD19−/−, BIL-10−/− and µMT mice displayed altered immunecell population frequencies in the blood and uterus with lower numbers of IL-10-secreting B cellsand T cells. BIL-10−/− mothers presented decreased frequencies of uterine CD4+CD25+Foxp3+ Tregcells. Co-stimulatory molecules are critical for feto-maternal tolerance and IL-10 secretion. We founddysregulated PD-1 expression in peripheral blood and ICOS expression in the uterus of CD19−/−,BIL-10−/− and µMT dams. Our data show that B cell-specific IL-10-signaling is essential for abalanced maternal immune response to an inflammatory stimulant that cannot be hampered withoutIL-10-secreting B cells.