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Interferon-γ Reduces Interleukin-4– and Interleukin-13–Augmented Transforming Growth Factor-β2 Production in Human Bronchial Epithelial Cells by Targeting Smads*

Fu-Qiang Wen, MD, PhD; Xiangde D. Liu, MD; Yusuke Terasaki; Qiuhong H. Fang, MD, PhD; Tetsu Kobayashi, MD, PhD; Shinji Abe, MD, PhD; Stephen I. Rennard, MD, FCCP
Author and Funding Information

*From the Pulmonary and Critical Care Medicine Section, University of Nebraska Medical Center, Omaha, NE.

Correspondence to: Stephen I. Rennard, MD, FCCP, Pulmonary and Critical Care Medicine Section, University of Nebraska Medical Center, 985125 Nebraska Medical Center, Omaha, NE 68198-5125; e-mail: srennard@unmc.edu



Chest. 2003;123(3_suppl):372S-373S. doi:10.1378/chest.123.3_suppl.372S
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The T-helper type 2 (Th2) cytokines, interleukin (IL)-4 and IL-13, and the T-helper type 1 cytokine interferon (IFN)-γ act differently in regulating airway inflammation and subepithelial fibrosis. The production of transforming growth factor (TGF)-β by airway epithelium and lung mesenchymal cells may be an important event in airway inflammation and remodeling. We hypothesized, therefore, that Th2 and T-helper type 1 cytokines may differentially regulate TGF-β production and may target TGF-β signaling.

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