The M2-type macrophage marker CCL18 was significantly increased in the serum and BAL of IPF patients, involved in the formation of fibrosis [35]; M2 macrophages can also produce TGF-β and PDGF to continuously activate fibroblasts and promote myofibroblast proliferation [36].The role of γδT cells in pulmonary fibrosis remains controversial. This evidence concerns the gene TGFB1 and pulmonary fibrosis.