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Infection and Immunity, January 2001, p. 213-220, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.213-220.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Activation of Valpha 14+ Natural Killer T Cells by alpha -Galactosylceramide Results in Development of Th1 Response and Local Host Resistance in Mice Infected with Cryptococcus neoformans

Kazuyoshi Kawakami,1,* Yuki Kinjo,1 Satomi Yara,1 Yoshinobu Koguchi,1 Kaori Uezu,1 Toshinori Nakayama,2 Masaru Taniguchi,2 and Atsushi Saito1

The First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Okinawa,1 and CREST (Core Research for Evolutional Science and Technology) Project, Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Chiba,2 Japan

Received 15 May 2000/Returned for modification 30 June 2000/Accepted 5 October 2000

We examined the effect of alpha -galactosylceramide (alpha -GalCer) on the synthesis of gamma interferon (IFN-gamma ) and local resistance in mice infected intravenously with Cryptococcus neoformans. The level of IFN-gamma in serum increased on day 3, reached a peak level on day 7, and decreased to the basal level on day 14 postinfection in mice treated with alpha -GalCer, while in vehicle-treated mice, no increase was detected at any time points except for a small increase on day 7. Such effects were not observed in NKT-KO mice. In CD4KO mice, minor synthesis of IFN-gamma was detected on day 3 in sera but was completely abolished by day 7. The alpha -GalCer-induced IFN-gamma production on day 3 was partially reduced in mice depleted of NK cells by treatment with anti-asialo-GM1 antibody (Ab). Spleen cells obtained from infected and alpha -GalCer-treated mice on day 7 produced a large amount of IFN-gamma upon restimulation with live organisms, while only a marginal level of production was detected in splenocytes from infected and vehicle-treated mice. Such effects were abolished in CD4KO and NKT-KO mice. Finally, the fungal loads in the lungs and spleen on days 7 and 14 were significantly reduced in alpha -GalCer-treated mice compared to those in control mice. In NKT-KO mice, local resistance elicited by alpha -GalCer was completely abolished, although no obvious exacerbation of infection was detected. Furthermore, treatment with anti-IFN-gamma monoclonal Ab mostly abrogated the protective effect of this agent. Thus, our results indicated that activation of Valpha 14+ NKT cells resulted in an increased Th1 response and local resistance to C. neoformans through production of IFN-gamma .

* Corresponding author. Mailing address: The First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan. Phone: 81(98) 895-1144. Fax: 81(98) 895-1414. E-mail: kawakami{at}med.u-ryukyu.ac.jp.

Infection and Immunity, January 2001, p. 213-220, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.213-220.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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