Autor: |
Chenuet, Pauline, Fauconnier, Louis, Madouri, Fahima, Marchiol, Tiffany, Rouxel, Nathalie, Ledru, Aurélie, Mauny, Pascal, Lory, Rachel, Uttenhove, Catherine, Snick, Jacques van, Yoichiro Iwakura, di Padova, Franco, Quesniaux, Valérie, Togbe, Dieudonnée, Ryffel, Bernhard |
Předmět: |
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Zdroj: |
Clinical Science; Oct2017, Vol. 131 Issue 20, p2533-2548, 16p |
Abstrakt: |
T helper (Th)17 immune response participates in allergic lung inflammation and asthma is reduced in the absence of interleukin (IL)-17 in mice. Since IL-17A and IL-17F are induced and bind the shared receptor IL-17RA, we asked whether both IL-17A and IL-17F contribute to house dust mite (HDM) induced asthma.We report that allergic lung inflammation is attenuated in absence of either IL-17A or IL-17F with reduced airway hyperreactivity, eosinophilic inflammation, goblet cell hyperplasia, cytokine and chemokine production as found in absence of IL-17RA. Furthermore, specific antibody neutralization of either IL-17A or IL-17F given during the sensitization phase attenuated allergic lung inflammation and airway hyperreactivity. In vitro activation by HDM of primary dendritic cells revealed a comparable induction of CXCL1 and IL-6 expression and the response to IL-17A and IL-17F relied on IL-17RA signaling via the adaptor protein act1 in fibroblasts. Therefore, HDM-induced allergic respiratory response depends on IL-17RA via act1 signaling and inactivation of either IL-17A or IL-17F is sufficient to attenuate allergic asthma in mice. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
Externí odkaz: |
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