Taken together, our results suggest that IL‐17 produced from Th17 (IL-17+CD4+) and γδ T cells could be the pivotal mediator for the development of BLM/NT127-infection-induced AE-IPF, and it promotes pulmonary inflammatory damage by recruiting neutrophils and eosinophils to the lung and inhibiting the response of pulmonary Treg cells (Figure 7). This evidence concerns the gene IL17A and idiopathic pulmonary fibrosis.