This increased expression appears to occur in the following manner: 1) MCP-1 may act as a profibrotic mediator by promoting fibroblast procollagen gene expression through the up-regulation of TGF-β1 [36]; and 2) TNF signaling through sTNF-receptors contributes to the regulation of TGF-β1 expression during BLM-induced lung fibrosis, as mice lacking sTNF-receptors have been shown to be resistant to BLM-induced lung fibrosis [30]. Here, CCL2 is linked to pulmonary fibrosis.