The time course of selected malarial infections in cytokine-deficient mice.

Abstract:

:Murine malarial parasites have long been characterized by their requirement for either antibody-mediated immunity (AMI) or cell-mediated immunity (CMI) for suppression of acute parasitemia, with Plasmodium yoelii reportedly requiring AMI for suppression and P. chabaudi requiring CMI. To assess this characterization in terms of the current T(H1)/T(H2)-CMI/AMI hypothesis, we infected gene-targeted "knockout" mice lacking either a type-1 cytokine (IL-2 or IFN-gamma) or a type-2 cytokine (IL-4 or IL-10) with one or the other species of Plasmodium. We observed that type-1 cytokine-deficient 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 infection with either parasite compared with that seen with their controls. We conclude that the mechanism of resolution of these well characterized 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 hypothesis.

journal_name

Exp Parasitol

authors

van der Heyde HC,Pepper B,Batchelder J,Cigel F,Weidanz WP

doi

10.1006/expr.1996.4132

subject

Has Abstract

pub_date

1997-02-01 00:00:00

pages

206-13

issue

2

eissn

0014-4894

issn

1090-2449

pii

S0014-4894(96)94132-6

journal_volume

85

pub_type

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