-19 is accompanied by loose interstitial fibrosis and can result in widespread fibrotic changes.79 IL-33 could also be important at these later stages of the disease. In a bleomycin-induced pulmonary fibrosis mouse model, the IL-33–ST2 axis is required to induce alternatively activated M2 macrophages and ILC2 to release key profibrotic cytokines.80 IL-33-activated mast cells might also play a role in organ fibrosis.81 Most remarkably, IL-33 has been shown to induce epithelial-to-mesechymal transition of type 2 pneumocytes through TGFβ signalling.82
IL-33 concentrations are elevated in patients with systemic sclerosis and correlate with the severity of pulmonary fibrosis, and patients with idiopathic