RECONSTITUTION OF B-CELL-DEPLETED MICE WITH B-CELLS RESTORES TH2-TYPEIMMUNE-RESPONSES DURING PLASMODIUM-CHABAUDI CHABAUDI INFECTION

In mice depleted dB cells from birth by treatment with anti-immunoglob ulin M(mu) antibodies, progression from a Th1- to a Th2-regulated immu ne response during primary infection viith Plasmodium chabaudi chabaud i fails to occur. While Th1-type immunity limits parasitemia, in the a bsence of B cells, chronic low-grade infections persist. Here, the sho w that reconstituting immune, and to a lesser extent naive, B cells to mice rendered deficient in B-cell function through anti-immunoglobuli n M(mu) pretreatment restores the CD4(+) T-cell response to the Th2 ty pe later in P. c. chabaudi infection and with it the capacity to elimi nate infection. This finding provides clear evidence that B cells are required for switching the balance of immune regulation between CD4(+) T cells from Th1 to Th2 during P. c. chabaudi infection and supports the concept that B cells, through antibody production, are needed for effective antimalarial immunity.