CD9 and infection: In murine models of malaria infection, primary P. chabaudi infection leads to expansion of short-lived, immature B220+ splenic plasma cells however secondary infection is accompanied by apparently normal emergence of a larger population of fully mature (Ighi, CD138hi, CD9+, B220−), terminally-differentiated B220- plasma cells in the bone marrow [31], indicating that memory B cells are efficiently induced by primary infection and are fully able to differentiate into long-lived plasma cells on secondary exposure to antigen.