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CUTTING EDGE |
14 NKT Cells Are Required for Allergen-Induced Airway Inflammation and Hyperreactivity in an Experimental Asthma Model1
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* Centre National de la Recherche Scientifique Formation de Recherche en Evolution 2444, Paris V, Hôpital Necker, Paris, France;
Unité de Pharmacologie Cellulaire, Institut Pasteur, Paris, France;
Departamento de Imunologia, Universidade de São Paulo, São Paulo, Brazil;
Institut National de la Santé et de la Recherche Médicale Unité 25 Hôpital Necker, Paris, France;
¶ La Jolla Institute for Allergy and Immunology, San Diego, CA 92121;
|| RIKEN Research Center for Allergy and Immunology and Graduate School of Medicine, Chiba University, Chiba, Japan;
# Section of Allergy and Clinical Immunology, Yale University School of Medicine, New Haven, CT 06520
Airway hyperreactivity (AHR), eosinophilic inflammation with a Th2-type cytokine profile, and specific Th2-mediated IgE production characterize allergic asthma. In this paper, we show that OVA-immunized J
18-/- mice, which are exclusively deficient in the invariant V14+ (iV14), CD1d-restricted NKT cells, exhibit impaired AHR and airway eosinophilia, decreased IL-4 and IL-5 production in bronchoalveolar lavage fluid, and reduced OVA-specific IgE compared with wild-type (WT) littermates. Adoptive transfer of WT iV14 NKT cells fully reconstitutes the capacity of J18-/- mice to develop allergic asthma. Also, specific tetramer staining shows that OVA-immunized WT mice have activated (CD69+) iV14 NKT cells. Importantly, anti-CD1d mAb treatment blocked the ability of iV14 T cells to amplify eosinophil recruitment to airways, and both Th2 cytokine and IgE production following OVA challenge. In conclusion, these findings clearly demonstrate that iV14 NKT cells are required to participate in allergen-induced Th2 airway inflammation through a CD1d-dependent mechanism.
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