Interestingly, full-length IL-33 can contribute to the pathogenesis of IPF by promoting the expression of cytokines such as TGF-β, interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), and tumor necrosis factor-alpha (TNF-α) (93). Here, CCL2 is linked to idiopathic pulmonary fibrosis.