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Journal Article

T Cell-Derived IL-17 Mediates Epithelial Changes in the Airway and Drives Pulmonary Neutrophilia


Schmidt-Supprian,  Marc
Schmidt-Supprian, Marc / Molecular Immunology and Signaltransduction, Max Planck Institute of Biochemistry, Max Planck Society;

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Fogli, L. K., Sundrud, M. S., Goel, S., Bajwa, S., Jensen, K., Derudder, E., et al. (2013). T Cell-Derived IL-17 Mediates Epithelial Changes in the Airway and Drives Pulmonary Neutrophilia. JOURNAL OF IMMUNOLOGY, 191(6), 3100-3111. doi:10.4049/jimmunol.1301360.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0017-9872-F
Th17 cells are a proinflammatory subset of effector T cells that have been implicated in the pathogenesis of asthma. Their production of the cytokine IL-17 is known to induce local recruitment of neutrophils, but the direct impact of IL-17 on the lung epithelium is poorly understood. In this study, we describe a novel mouse model of spontaneous IL-17-driven lung inflammation that exhibits many similarities to asthma in humans. We have found that STAT3 hyperactivity in T lymphocytes causes an expansion of Th17 cells, which home preferentially to the lungs. IL-17 secretion then leads to neutrophil infiltration and lung epithelial changes, in turn leading to a chronic inflammatory state with increased mucus production and decreased lung function. We used this model to investigate the effects of IL-17 activity on airway epithelium and identified CXCL5 and MIP-2 as important factors in neutrophil recruitment. The neutralization of IL-17 greatly reduces pulmonary neutrophilia, underscoring a key role for IL-17 in promoting chronic airway inflammation. These findings emphasize the role of IL-17 in mediating neutrophil-driven pulmonary inflammation and highlight a new mouse model that may be used for the development of novel therapies targeting Th17 cells in asthma and other chronic pulmonary diseases.