TGFB1 and idiopathic pulmonary fibrosis: In particular, during IPF progression, both the resident and recruited alveolar AMs undergo M2-like macrophages polarization [82], upregulating CCL-18 that triggers excessive collagen deposition from lung resident fibroblasts [83], TLR2 pathways [84], TGF-β1 [85], and apoptosis resistance [86].