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

doi:10.1128/IAI.69.1.213-220.2001

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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 V $alpha$ 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 resistancein mice infected intravenously with Cryptococcus neoformans. Thelevel of IFN- $gamma$ in serum increased on day 3, reached a peak levelon day 7, and decreased to the basal level on day 14 postinfectionin mice treated with $alpha$ -GalCer, while in vehicle-treated mice,no increase was detected at any time points except for a smallincrease on day 7. Such effects were not observed in NKT-KO mice.In CD4KO mice, minor synthesis of IFN- $gamma$ was detected on day 3in sera but was completely abolished by day 7. The $alpha$ -GalCer-inducedIFN- $gamma$ production on day 3 was partially reduced in mice depletedof NK cells by treatment with anti-asialo-GM₁ antibody (Ab). Spleencells obtained from infected and $alpha$ -GalCer-treated mice on day7 produced a large amount of IFN- $gamma$ upon restimulation with liveorganisms, while only a marginal level of production was detectedin splenocytes from infected and vehicle-treated mice. Such effectswere abolished in CD4KO and NKT-KO mice. Finally, the fungal loadsin the lungs and spleen on days 7 and 14 were significantly reducedin $alpha$ -GalCer-treated mice compared to those in control mice. InNKT-KO mice, local resistance elicited by $alpha$ -GalCer was completelyabolished, although no obvious exacerbation of infection was detected.Furthermore, treatment with anti-IFN- $gamma$ monoclonal Ab mostly abrogatedthe protective effect of this agent. Thus, our results indicatedthat activation of V $alpha$ 14⁺ NKT cells resulted in an increased Th1 response and local resistanceto 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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Activation of V14+ Natural Killer T Cells by -Galactosylceramide Results in Development of Th1 Response and Local Host Resistance in Mice Infected with Cryptococcus neoformans

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