In mice infected with Klebsiella pneumoniae, IL-22 can promote epithelial repair, inhibit epithelial damage, and thus inhibit the inflammatory response; in mice infected with chlamydia pneumoniae, IL-22 can participate in host defense against chlamydia infection by regulating Th1/Th17 [46]; the expression of IL-22 was decreased in bleomycin-induced pulmonary fibrosis in mice [47], indicating that IL-22 may have a protective effect, which is consistent with our conclusion that IL-22 can inhibit the development of pulmonary fibrosis. This evidence concerns the gene IL22 and pulmonary fibrosis.