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Infection and Immunity, October 2006, p. 5903-5913, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00311-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Rapid Development of a Gamma Interferon-Secreting Glycolipid/CD1d-Specific V{alpha}14+ NK1.1– T-Cell Subset after Bacterial Infection

Masashi Emoto,1,2* Izumi Yoshizawa,1 Yoshiko Emoto,1,2 Mamiko Miamoto,1 Robert Hurwitz,3 and Stefan H. E. Kaufmann1

Department of Immunology, Max Planck Institute for Infection Biology, D-10117 Berlin, Germany,1 Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Maebashi, Gunma 371-8511, Japan,2 Central Support Unit Biochemistry, Max Planck Institute for Infection Biology, D-10117 Berlin, Germany3

Received 24 February 2006/ Returned for modification 1 May 2006/ Accepted 16 July 2006

The phenotypic and functional changes of glycolipid presented by CD1d(glycolipid/CD1d) specific V{alpha}14+ T cells in the liver of mice at early stages of bacterial infection were investigated. After Listeria monocytogenes infection or interleukin-12 (IL-12) treatment, {alpha}-galactosylceramide/CD1d tetramer-reactive ({alpha}-GalCer/CD1d+) T cells coexpressing natural killer (NK) 1.1 marker became undetectable and, concomitantly, cells lacking NK1.1 emerged in both euthymic and thymectomized animals. Depletion of the NK1.1+ subpopulation prevented the emergence of {alpha}-GalCer/CD1d+ NK1.1– T cells. Before infection, NK1.1+, rather than NK1.1–, {alpha}-GalCer/CD1d+ T cells coexpressing CD4 were responsible for IL-4 production, whereas gamma interferon (IFN-{gamma}) was produced by cells regardless of NK1.1 or CD4 expression. After infection, IL-4-secreting cells became undetectable among {alpha}-GalCer/CD1d+ T cells, but considerable numbers of IFN-{gamma}-secreting cells were found among NK1.1–, but not NK1.1+, cells lacking CD4. Thus, NK1.1 surface expression and functional activities of V{alpha}14+ T cells underwent dramatic changes at early stages of listeriosis, and these alterations progressed in a thymus-independent manner. In mutant mice lacking all {alpha}-GalCer/CD1d+ T cells listeriosis was ameliorated, suggesting that the subtle contribution of the NK1.1– T-cell subset to antibacterial protection is covered by more profound detrimental effects of the NK1.1+ T-cell subset.

* Corresponding author. Mailing address: Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan. Phone: 81-27-220-8935. Fax: 81-27-220-8935. E-mail: memoto{at}health.gunma-u.ac.jp.

Editor: J. L. Flynn

Infection and Immunity, October 2006, p. 5903-5913, Vol. 74, No. 10
0019-9567/06/$08.00+0     doi:10.1128/IAI.00311-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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