Maternal schistosomiasis impairs offspring Interleukin-4 production and B cell expansion

Epidemiological studies have identified a correlation between maternal helminth infections and reduced immunity to some early childhood vaccinations, but the cellular basis for this is poorly understood. Here, we investigated effects of Schistosoma mansoni infection on steady-state offspring immunity, as well induced by commercial tetanus/diphtheria vaccine using dual IL-4 reporter mouse model schistosomiasis. We demonstrate that born S . infected mothers circulating plasma cells peripheral lymph node follicular dendritic at steady state. These reductions correlate with production iNKT cells, source in during life. defects were maintained long-term secretion germinal center generation TFH, memory B, T response immunization tetanus/diphtheria. Using single-cell RNASeq following offspring, defect cell-cycle cell-proliferation pathways addition reduction Ebf-1, key B-cell transcription factor, majority B cells. are dependent presence egg antigens mother, single-sex do not these transcriptional defects. data indicate schistosomiasis leads antigen-induced first time provide mechanistic insight into factors regulating mothers.