Methods: We developed six-color flow cytometry panels to differentiate subpopulations of B cells from cord blood mononuclear cells (CBMC) isolated from North American and Kenyan neonates. North American neonates had no prenatal chronic infectious exposures. Kenyan neonates examined had evidence of prenatal HIV, cytomegalovirus (CMV), P falciparum malaria or no infectious exposures. Proportions of B cell subpopulations were compared between the exposure groups. Additionally, we examined the ability of B cells in each group to respond to polyclonal activation in culture.
Results: We found that neonates exposed to chronic prenatal infections (HIV, CMV and malaria) displayed higher levels of atypical (CD19+CD27-CD21-IgD-) and activated (CD19+CD27+CD21-IgD-) memory B cells compared to Kenyan non-exposed and North American neonates. Little differences were appreciated in naive B cell (CD19+CD21+CD27-CD10-) or classic isotype switched memory B cell (CD19+CD27+CD21+IgD-) populations. Neonates exposed to HIV had a lower proportion of CD5+ B cell compared to all other groups. Polyclonal activation of B cells resulted in subtle shifts in CD5 and TLR2 expression, which were similar among the exposure groups.
Conclusion: The results of our study suggest that the presence of chronic infections during pregnancy affects B cell development, leading to increased levels of atypical and activated memory B cells. The resultant changes may affect the infant’s susceptibility to infections and will need to be further investigated