4.6 Article

Induction of Airway Hyperreactivity by IL-25 Is Dependent on a Subset of Invariant NKT Cells Expressing IL-17RB

Journal

JOURNAL OF IMMUNOLOGY
Volume 182, Issue 8, Pages 5116-5122

Publisher

AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0804213

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Funding

  1. National Institutes of Health [R01 A1066020]
  2. German Research Foundation (DFG) [STO 467/4-2]

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IL-25 has been shown to induce Th2 responses and airway hyperreactivity (AHR) in mice, but the mechanism of action is not understood and it is unclear which cells mediate this disease. In this study we show that the receptor for IL-25, IL-17RB, is highly expressed on a subset of naive and activated CD4+ invariant NKT (iNKT) cells, but not on activated T cells. IL-17RB(+) iNKT cells produced large amounts of Th2 cytokines that were substantially increased by IL-25 stimulation. Furthermore, IL-17RB(+) iNKT cells were capable of restoring AHR in iNKT cell-deficient mice, whereas IL-17RB(-) iNKT cells failed to reconstitute AHR and lung inflammation. Finally, IL-17RB(+) iNKT cells were detected in the lungs of wild-type mice, and induction of AHR by intranasal administration of IL-25 was significantly impaired in iNKT cell-deficient mice. Overall, our data suggest a critical role for iNKT cells in IL-25-mediated AHR. These results may lead to novel therapeutic approaches to target IL-17RB(+) iNKT cells for the treatment of allergic asthma. The Journal of Immunology, 2009, 182: 5116-5122.

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