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

a1 Department of Veterinary Parasitology, University of Glasgow, Glasgow, UK
a2 Division of Infection and Immunity, University of Glasgow, Glasgow, UK
a3 Department of Immunology, University of Strathclyde, Glasgow, UK


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.

(Received April 1 2000)
(Revised May 20 2000)
(Accepted May 23 2000)

Key Words: IFNγ; IL-4; Plasmodium chabaudi; lymphomyeloid cells; liver.

c1 Corresponding author: Department of Veterinary Parasitology, University of Glasgow, Bearsden Road, Glasgow G61 1QH. Tel: +44 141 330 5751. Fax: +44 141 330 5603. E-mail: