malaria in B cell-deficient mice

Abstract: 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 y T 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}43T 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 y T 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 intac