Collaborative Interactions between Type 2 Innate Lymphoid Cells and Antigen-Specific CD4+ Th2 Cells Exacerbate Murine Allergic Airway Diseases with Prominent Eosinophilia

摘要: Type-2 innate lymphoid cells (ILC2s) and the acquired CD4(+) Th2 Th17 contribute to pathogenesis of experimental asthma; however, their roles in Ag-driven exacerbation chronic murine allergic airway diseases remain elusive. In this study, we report that repeated intranasal rechallenges with only OVA Ag were sufficient trigger hyperresponsiveness, prominent eosinophilic inflammation, significantly increased serum OVA-specific IgG1 IgE rested mice previously developed diseases. The recall response inoculation preferentially triggered a further increase lung cells, whereas ILC2 cell numbers remained constant. Furthermore, Stat6(-/-)/IL-17-GFP mice, or ILC2s T cell-ablated failed mount an Ag. After rechallenge ablation, loss resulted enhanced reduced IL-13 production by IL-25 IL-33 stimulation, respectively. return, Ag-mediated proliferation cocultured cytokine production, promoted inflammation goblet hyperplasia driven adoptively transferred Ag-specific cells. Thus, these results suggest recurring exposures triggers which facilitates collaborative interactions between drive phenotype.