The time course of selected malarial infections in cytokine-deficient
mice. Experimental Parasitology 85, 206-213. Murine malarial parasites
have long been characterized by their requirement for either antibody
-mediated immunity (AMI) or cell-mediated immunity (CMI) for suppressi
on of acute parasitemia, with Plasmodium yoelii reportedly requiring A
MI for suppression and P. chabaudi requiring CMI. To assess this chara
cterization in terms of the current T-H1/T-H2-CMI/AMI hypothesis, we i
nfected gene-targeted ''knockout'' mice lacking either a type-1 cytoki
ne (IL-2 or IFN-gamma) or a type-2 cytokine (IL-4 or IL-10) with one o
r the other species of Plasmodium. We observed that type-1 cytokine-de
ficient mice developed exacerbated malaria with either P. yoelii or P.
chabaudi, compared with that seen in heterozygote controls. Moreover,
type-2 cytokine knockout mice showed a similar time course of infecti
on with either parasite compared with that seen with their controls. W
e conclude that the mechanism of resolution of these well characterize
d malarial infections cannot be linked definitely to these T-H1- and T
-H2-associated cytokines as predicted by the T-H1/T-H2-CMI/AMI hypothe
sis. (C) 1997 Academic Press.