Thirdly, the reprogrammed M2-type macrophage could secrete CCL9 to recruit and stimulate Th17 cells to secrete IL-17A thus aggravating immune disorder, and simultaneously stimulate Tgf-β to activate fibroblast and further differentiated into myofibroblasts aggravating IPF damage (Figure 5 and 6). The gene discussed is IL17A; the disease is idiopathic pulmonary fibrosis.