Collectively, production of IL-22 from pulmonary CD4+ T cells is affected by IL-17 in BLM/NT127-induced AE-IPF, and the increased expression of IL-22 in the absence of IL-17 may have contributed to the protection against airway damage, but the definitive role of IL-22 in AE-IPF remains to be determined. Here, CD4 is linked to idiopathic pulmonary fibrosis.