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International Immunology, Vol. 12, No. 8, 1117-1125, August 2000
© 2000 Japanese Society for Immunology

Schistosoma mansoni infection cancels the susceptibility to Plasmodium chabaudi through induction of type 1 immune responses in A/J mice

Ayako Yoshida1,2, Haruhiko Maruyama1, Takashi Kumagai1, Teruaki Amano3, Fumie Kobayashi4, Manxin Zhang5, Kunisuke Himeno5 and Nobuo Ohta1

1 Department of Medical Zoology, Nagoya City University Medical School, 1 Azakawasumi, Mizuhocho, Mizuhoku, Nagoya 467-8601, Japan
2 Japan Health Sciences Foundation, Tokyo 103-0001, Japan
3 Department of Parasitology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan
4 Department of Tropical Medicine and Parasitology, Kyorin University School of Medicine, Mitaka 181-8611, Japan
5 Department of Parasitology, Tokushima University School of Medicine, Tokushima 770-8503, Japan

Correspondence to: N. Ohta

Susceptibility to Plasmodium chabaudi depends on the relative dominance of Th1/Th2 responses in host mice. A Th2-dominant response during the early phase of infection in susceptible A/J mice causes a fatal disease course due to severe malaria. Schistosoma mansoni is a potent inducer of a Th2-dominant response not only to the parasite antigens, but also to other antigens concurrently existing in the host animals. In spite of S. mansoni infection, these A/J mice escape death from malaria and showed accompanied enhanced production of IFN-{gamma} to malaria antigens. Treatment with anti-IFN-{gamma} mAb in S. mansoni-infected A/J mice abolished the resistance to malaria, indicating that IFN-{gamma} was responsible for the resistance to P. chabaudi in S. mansoni-infected A/J mice. Results in this study show that under certain circumstances, S. mansoni infection can promote type 1 immune responses in A/J mice that normally develop Th2 responses.

Keywords: HSP 90, IFN-{gamma}, Plasmodium chabaudi, Schistosoma mansoni, Th1/Th2

Transmitting editor: K. Okumura


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