malaria in B cell-deficient mice

Mice rendered B cell-deficient either by chronic anti-j.t treatment initiated at birth or by gene knockout (JHD and j.t-MT mice) suppressed acute Plasmodium chabaudi infections with a time course similar to intact control mice. Moreover, both kinds of B cell-deficient mice showed a 50- to 100-fold increase in splenic y#{246} T cell number after suppression of parasitemia compared with uninfected B cell-de- ficient controls; the magnitude of this increase re- suited in significantly (P< 0.05) greater numbers of splemc 'y#{246} T cells in the B cell-deficient mice than in infected B cell-intact controls (about 10-fold). In contrast, the number of splenic CD4+ � T cells was only slightly elevated ( < 2-fold) in both kinds of B cell-deficient mice compared with their intact con- trols. The number of splenic yT cells following suppression of P. vinckei parasitemia was approxi- mately ninefold greater in JHD mice than in C57BL/6 controls, whereas similar numbers of splenic CD4+ #{128}43 T cells were detected. Maximal numbers of y#{246} T cells were in cell-cycle in both JHD and C57B116 mice during descending P. chabaudi parasitemia, but the number of y6 T cells in cell-cycle was greater in B cell-deficient mice than in intact controls. Inter- leukin-lO (IL-lO), a potent TH1 cell-suppressive molecule, does not appear to down-regulate the yT cell response during malaria in B cell-intact mice because the magnitude of the 'y#{246} T cell response was not significantly greater in IL-lO knockout mice compared with heterozygote controls. These findings collectively indicate that a markedly enhanced cx- pansion of the y6 T cell population occurs in the absence of B cells, and this expansion occurs pre- dominantly during acute malaria when parasite bur- dens are similar in B cell-deficient animals and intact controls. J. Leukoc. Biol. 60: 221-229; 1996.