IL-33 concentrations are elevated in patients with systemic sclerosis and correlate with the severity of pulmonary fibrosis, and patients with idiopathic pulmonary fibrosis show increased serum concentrations of soluble ST2 when the disease is exacerbated.82 IL-33 can induce cytokines (eg, TGFβ, IL-13) and chemokines (eg, CCL2, CXCL6) involved in pulmonary fibrosis, which are also increased in patients infected with SARS-CoV-2,6, 9, 11, 15, 26 thus suggesting additional roles for IL-33 in driving the post-acute fibrotic phase of COVID-19. Growth factors such as vascular endothelial growth factor, platelet-derived growth factor, and fibroblast growth factor are all involved in fibrotic processes and are overexpressed in patients with COVID-19,9 and γδ T cells exposed to TGFβ might produce connective tissue growth factor (figure 2).83