| First Author | Nieuwenhuizen NE | Year | 2018 |
| Journal | Sci Rep | Volume | 8 |
| Issue | 1 | Pages | 885 |
| PubMed ID | 29343807 | Mgi Jnum | J:260140 |
| Mgi Id | MGI:6148366 | Doi | 10.1038/s41598-017-19060-9 |
| Citation | Eva Nieuwenhuizen N, et al. (2018) House dust mite induced allergic airway disease is attenuated in CD11c(cre)IL-4Ralpha(-/l) degrees (x) mice. Sci Rep 8(1):885 |
| abstractText | The precise mechanisms leading to development of T helper type (Th)2-driven allergic responses are unknown. We aimed to determine how IL-4 receptor alpha (IL-4Ralpha) signaling on CD11c(+) cells influences allergen-induced Th2 responses in mice. CD11c(cre)IL-4Ralpha(-/l) degrees (x) mice, deficient in IL-4Ralpha on dendritic cells and alveolar macrophages, were compared to IL-4Ralpha(-/l) degrees (x) littermate controls in models of allergic airway disease induced by OVA/alum, OVA alone or house dust mite. Cytokine responses, eosinophil and neutrophil infiltration into the lungs, airway hyperreactivity and mucus hypersecretion were evaluated after allergen challenge. In the OVA/alum model, CD11c(cre)IL-4Ralpha(-/lox) mice had similar airway hyperreactivity, eosinophil infiltration, Th2-type cytokine production and mucus hypersecretion to littermate controls. When alum was omitted during sensitization, CD11c(cre)IL-4Ralpha(-/lox) mice had similar airway hyperreactivity and mucus secretion but reduced Th2-type cytokine production and eosinophils, suggesting alum overrides the requirement for IL-4Ralpha signaling on CD11c(+) cells in enhancing Th2-type responses. In the house dust mite model, CD11c(cre)IL-4Ralpha(-/lox) mice showed similar mucus secretion, but reduced Th2 responses, eosinophils, neutrophils and airway hyperreactivity, unlike previously tested LysM(cre)IL-4Ralpha(-/lox) mice, which lack IL-4Ralpha on alveolar macrophages but not on dendritic cells. Therefore, our results indicate that IL-4Ralpha signaling on dendritic cells promotes allergen-induced Th2 responses and eosinophil infiltration into the lung. |
