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Infection and Immunity, March 2003, p. 1234-1241, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1234-1241.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Activation of Natural Killer T Cells by {alpha}-Galactosylceramide Impairs DNA Vaccine-Induced Protective Immunity against Trypanosoma cruzi

Yasushi Miyahira,1* Masaharu Katae,1,2 Kazuyoshi Takeda,3 Hideo Yagita,3 Ko Okumura,3 Seiki Kobayashi,4 Tsutomu Takeuchi,4 Tsuneo Kamiyama,5 Yoshinosuke Fukuchi,2 and Takashi Aoki1

Department of Molecular and Cellular Parasitology,1 Department of Respiratory Medicine,2 Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421,3 Department of Tropical Medicine and Parasitology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582,4 Department of Veterinary Sciences, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan5

Received 2 August 2002/ Returned for modification 3 October 2002/ Accepted 14 November 2002

Innate immunity as a first defense is indispensable for host survival against infectious agents. We examined the roles of natural killer (NK) T cells in defense against Trypanosoma cruzi infection. The T. cruzi parasitemia and survival of CD1d-deficient mice exhibited no differences compared to wild-type littermates. NK T-cell activation induced by administering {alpha}-galactosylceramide ({alpha}-GalCer) to T. cruzi-infected mice significantly changed the parasitemia only in the late phase of infection and slightly improved survival when mice were infected intraperitoneally. The combined usage of {alpha}-GalCer and benznidazole, a commercially available drug for Chagas' disease, did not enhance the therapeutic efficacy of benznidazole. These results suggest that NK T cells do not play a pivotal role in resistance to T. cruzi infection. In addition, we found that the coadministration of {alpha}-GalCer with DNA vaccine impaired the induction of epitope-specific CD8+ T cells and undermined the DNA vaccine-induced protective immunity against T. cruzi. Our results, in contrast to previous reports demonstrating the protective roles of NK T cells against other infectious agents, suggest that these cells might even exhibit adverse effects on vaccine-mediated protective immunity.

* Corresponding author. Mailing address: Department of Molecular and Cellular Parasitology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. Phone: 81-3-5802-1043. Fax: 81-3-5800-0476. E-mail: miyahira{at}med.juntendo.ac.jp.

Editor: J. M. Mansfield

Infection and Immunity, March 2003, p. 1234-1241, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1234-1241.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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