B cells and
antibodies are essential for the protective immune response against a blood-stage
Plasmodium infection. Although extensive research has focused on memory as well as plasma B-cell responses during
infection, little is known about how
malaria affects B-cell development and splenic maturation into marginal zone B (MZB) and follicular B (FoB) cells. In this study, we show that acute Plasmodium chabaudi AS
infection in C57Bl/6 mice causes severe disruption of B lymphopoiesis in the bone marrow, affecting in particular pro-, pre-, and immature B cells as well as the expression of the bone marrow B-cell retention
chemokine CXCL12. In addition, elevated apoptosis of transitional T2 and marginal zone (MZ) B cells was observed during and subsequent to the control of the first wave of
parasitemia. In contrast, Folllicular (Fo) B cells levels were retained in the spleen throughout the
infection, suggesting that these are essential for parasite clearance and proper infection control.