The Journal of Experimental Medicine
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Published online April 30, 2007
doi:10.1084/jem.20061551
The Journal of Experimental Medicine, Vol. 204, No. 5, 995-1001
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Michel et al.
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BRIEF DEFINITIVE REPORT

 Identification of an IL-17–producing NK1.1neg iNKT cell population involved in airway neutrophilia

Marie-Laure Michel1, Alexandre Castro Keller1, Christophe Paget2,3, Masakazu Fujio4,5, François Trottein2,3, Paul B. Savage6, Chi-Huey Wong4,5, Elke Schneider1, Michel Dy1, and Maria C. Leite-de-Moraes1

1 Unité Mixte de Recherche 8147, Centre National de la Recherche Scientifique, Faculté de Médecine René Descartes, Paris V, Hôpital Necker, 75743 Paris, Cedex 15, France
2 Institut National de la Santé et de la Recherche Médicale, U547, F-59019 Lille, France
3 Institut Pasteur de Lille, Institut Fédératif de Recherche 142, F-59019 Lille, France
4 Department of Chemistry and 5 The Skaggs Institute for Chemical Biology, Scripps Research Institute, La Jolla, CA 92037
6 Department of Chemistry and Biochemistry, Brigham Young University, Provo, UT 84602

CORRESPONDENCE Maria C. Leite-de-Moraes: leite.de.moraes{at}necker.fr

Invariant natural killer T (iNKT) cells are an important source of both T helper type 1 (Th1) and Th2 cytokines, through which they can exert beneficial, as well as deleterious, effects in a variety of inflammatory diseases. This functional heterogeneity raises the question of how far phenotypically distinct subpopulations are responsible for such contrasting activities. In this study, we identify a particular set of iNKT cells that lack the NK1.1 marker (NK1.1neg) and secrete high amounts of interleukin (IL)-17 and low levels of interferon (IFN)-{gamma} and IL-4. NK1.1neg iNKT cells produce IL-17 upon synthetic ({alpha}-galactosylceramide [{alpha}-GalCer] or PBS-57), as well as natural (lipopolysaccharides or glycolipids derived from Sphingomonas wittichii and Borrelia burgdorferi), ligand stimulation. NK1.1neg iNKT cells are more frequent in the lung, which is consistent with a role in the natural immunity to inhaled antigens. Indeed, airway neutrophilia induced by {alpha}-GalCer or lipopolysaccharide instillation was significantly reduced in iNKT-cell–deficient J{alpha}18–/– mice, which produced significantly less IL-17 in their bronchoalveolar lavage fluid than wild-type controls. Furthermore, airway neutrophilia was abolished by a single treatment with neutralizing monoclonal antibody against IL-17 before {alpha}-GalCer administration. Collectively, our findings reveal that NK1.1neg iNKT lymphocytes represent a new population of IL-17–producing cells that can contribute to neutrophil recruitment through preferential IL-17 secretion.


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