To summarise, through direct and indirect transwell co-cultures as well as CM experiments, it has been shown that the interaction between lung fibroblasts and macrophages lead to the release of cytokines and chemokines (e.g. CCL18, CCL2, CX3CL1 and CXCL10) that act as chemoattractants for immune cells that ultimately contribute to the inflammatory mechanisms involved in IPF chronic remodeling [42, 43, 65]. This evidence concerns the gene CCL18 and idiopathic pulmonary fibrosis.