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Escape of malaria parasites from host immunity requires CD4+CD25+ regulatory T cells

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Abstract

Infection with malaria parasites frequently induces total immune suppression, which makes it difficult for the host to maintain long-lasting immunity. Here we show that depletion of CD4+CD25+ regulatory T cells (Treg) protects mice from death when infected with a lethal strain of Plasmodium yoelii, and that this protection is associated with an increased T-cell responsiveness against parasite-derived antigens. These results suggest that activation of Treg cells contributes to immune suppression during malaria infection, and helps malaria parasites to escape from host immune responses.

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Figure 1: Immunosuppression in PyL-infected mice.
Figure 2: Adverse contribution of Treg cells in protection to infection with PyL.

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Acknowledgements

We thank M. Tsubosaka, N. Kanbe, K. Ishii and S. Hamano for assistance with experiments, and J.R. Dorfman for helpful comments. This work was supported by grants-in-aid from the Ministry of Education, Culture, Sports, Science and Technology in Japan and the Industrial Technology Research Grant Program from NEDO of Japan (to K.Y.). The experiments were approved by the animal care committee of the University of Tokushima.

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Authors and Affiliations

  1. Department of Immunology & Parasitology, School of Medicine, The University of Tokushima, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan

    Hajime Hisaeda, Yoichi Maekawa, Daiji Iwakawa, Hiroko Okada, Kenji Kishihara, Shin-ichi Tsukumo & Koji Yasutomo

  2. Department of Parasitology, Faculty of Medical Sciences, Kyushu University, 3 Maidashi, East Ward Fukuoka, 812-8582, Japan

    Kunisuke Himeno

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  1. Hajime Hisaeda
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  2. Yoichi Maekawa
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  3. Daiji Iwakawa
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  4. Hiroko Okada
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  5. Kunisuke Himeno
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  6. Kenji Kishihara
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  7. Shin-ichi Tsukumo
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  8. Koji Yasutomo
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Correspondence to Koji Yasutomo.

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Hisaeda, H., Maekawa, Y., Iwakawa, D. et al. Escape of malaria parasites from host immunity requires CD4+CD25+ regulatory T cells. Nat Med 10, 29–30 (2004). https://doi.org/10.1038/nm975

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  • DOI: https://doi.org/10.1038/nm975

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