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Protective immunity to erythrocytic Plasmodium chabaudi AS infection involves IFNγ-mediated responses and a cellular infiltrate to the liver

Published online by Cambridge University Press:  02 January 2001

P. BALMER
Affiliation:
Department of Veterinary Parasitology, University of Glasgow, Glasgow, UK
J. ALEXANDER
Affiliation:
Department of Immunology, University of Strathclyde, Glasgow, UK
R. S. PHILLIPS
Affiliation:
Division of Infection and Immunity, University of Glasgow, Glasgow, UK
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Abstract

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IFNγ receptor (IFNγR) deficient mice and IL-4 deficient mice were infected with blood-stage Plasmodium chabaudi AS in order to analyse the role of Th1 (IFNγ) and Th2 (IL-4)-associated cytokines in the development of protective immunity to the parasite. A high mortality rate and failure to reduce the primary parasitaemia to subpatent levels was observed in the IFNγR deficient mice. IL-4 deficient mice controlled a primary P. chabaudi AS infection in a similar manner to control mice and no mortality was observed. IFNγR deficient mice had a reduction in parasite-specific IgG and a significantly increased level of total IgE compared to control mice. There was no reduction in the level of parasite-specific IgG in IL-4 deficient mice. Cytological analysis of the cells present in the spleen and liver during the primary parasitaemia revealed a reduction in the numbers of lymphocytes, monocytes and polymorphonuclear (PMN) cells in the liver at the peak of parasitaemia in both IFNγR deficient mice and IL-4 deficient mice compared to control mice. Adoptive transfer studies demonstrated that cells isolated from the liver at day 11 post-infection could confer some protective immunity to P. chabaudi AS infection.

Type
Research Article
Copyright
2000 Cambridge University Press