In this study, we found that (1) a distinct population of lung-resident pathogenic Siglec-F+ neutrophils exists in mice with PPE-induced emphysema and that (2) lung-resident γδ+ T-cell-derived IL-17A stimulates lung airway epithelial/stromal cells to produce G-CSF, which drives the development of Siglec-F+ neutrophils through the JAK2/STAT3, PI3K-independent mTOR, and p38 MAPK signaling pathways, ultimately contributing to the development of emphysema and symptom exacerbation. The gene discussed is JAK2; the disease is pulmonary emphysema.