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). The gene discussed is CD4; the disease is idiopathic pulmonary fibrosis.