Alternatively activated (M2) macrophages, the predominant macrophage phenotype in the lungs of IPF patients, have an impaired innate immune function but produce fibrogenic mediators such as TGF-β, IL-13, and chemokine (C-C motif) ligand 18 (CCL18; Pechkovsky et al., 2010). This evidence concerns the gene CCL18 and idiopathic pulmonary fibrosis.