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IL-17A produced by αβ T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction
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IL-17A produced by αβ T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction
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Journal Article
IL-17A produced by αβ T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction
2012
Overview
IL-17 is associated with asthma, and T
H
H17 cells are found in the airways of individuals with asthma. Dean Sheppard and his colleagues now report that IL-17A (but not IL-17F) directly enhances contractile responses in airway smooth muscle cells. Mice lacking T
H
17 cells in the lungs exhibit reduced airway hyper-responsiveness in response to allergen challenge.
Emerging evidence suggests that the T helper 17 (T
H
17) subset of αβ T cells contributes to the development of allergic asthma. In this study, we found that mice lacking the αvβ8 integrin on dendritic cells did not generate T
H
17 cells in the lung and were protected from airway hyper-responsiveness in response to house dust mite and ovalbumin sensitization and challenge. Because loss of T
H
17 cells inhibited airway narrowing without any obvious effects on airway inflammation or epithelial morphology, we examined the direct effects of T
H
17 cytokines on mouse and human airway smooth muscle function. Interleukin-17A (IL-17A), but not IL-17F or IL-22, enhanced contractile force generation of airway smooth muscle through an IL-17 receptor A (IL-17RA)–IL-17RC, nuclear factor κ light-chain enhancer of activated B cells (NF-κB)–ras homolog gene family, member A (RhoA)–Rho-associated coiled-coil containing protein kinase 2 (ROCK2) signaling cascade. Mice lacking integrin αvβ8 on dendritic cells showed impaired activation of this pathway after ovalbumin sensitization and challenge, and the diminished contraction of the tracheal rings in these mice was reversed by IL-17A. These data indicate that the IL-17A produced by T
H
17 cells contributes to allergen-induced airway hyper-responsiveness through direct effects on airway smooth muscle.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 692/698/1543/1565/1597/554/1898/1273
/ Animals
/ Asthma
/ Biomedical and Life Sciences
/ Dendritic Cells - metabolism
/ Dose-Response Relationship, Drug
/ Enzyme Inhibitors - pharmacology
/ Humans
/ Interleukin-17 - pharmacology
/ Male
/ Methacholine Chloride - pharmacology
/ Mice
/ Muscarinic Agonists - pharmacology
/ Muscle Contraction - drug effects
/ Muscle Contraction - physiology
/ Muscle, Smooth - drug effects
/ Potassium Chloride - pharmacology
/ Respiratory System - cytology
/ rho-Associated Kinases - metabolism
/ rhoA GTP-Binding Protein - metabolism
/ Signal Transduction - drug effects
/ T cells
