Nrp1 downregulation correlates with enhanced ILC2 responses during IL-33 challenge

Group 2 innate lymphoid cells (ILC2s) play critical roles in driving the pathogenesis of allergic airway inflammation. The mechanisms underlying the regulation of ILC2s remain to be fully understood. Here, we identified neuropilin-1 (Nrp1) as a surface marker of ILC2s in response to IL-33 stimulation. Nrp1 was abundantly expressed in ILC2s from lung under steady state, which was significantly reduced upon IL-33 stimulation. ILC2s with high expression of Nrp1 (Nrp1high) displayed lower response to IL-33, as compared with Nrp1low ILC2s. Transcriptional profiling and flow cytometric analysis showed that downregulation of AKT-mTOR signaling participated in the diminished functionality of Nrp1high ILC2s. These observations revealed a potential role of Nrp1 in ILC2s responses under allergic inflammatory condition. To evaluate the transcriptional differences between Nrp1high and Nrp1low ILC2s , we sorted Nrp1high and Nrp1low ILC2s from lungs at IL-33 treatment condition. We then performed gene expression by KEGG analysis, Heat map analysis and volcano plot analysis