Transcriptomic analyses of bronchoalveolar lavage fluid from patients with COVID-19 have revealed a strong upregulation of IL-33.11 IL-33 is a cytokine of the IL-1 family that is expressed in barrier tissues and exerts pleiotropic functions. In the lungs, IL-33 is promptly released, mainly by injured epithelial alveolar cells, following infection and cellular damage.12 Among its functions, IL-33 enhances TGFβ-mediated differentiation of Foxp3+ regulatory T (Treg) cells13 and stimulates CD11c+ myeloid dendritic cells to secrete IL-2, which drives Treg cell expansion, thus ultimately promoting resolution of inflammation.14 Individuals infected with SARS-CoV-2 who develop milder symptoms tend to have large numbers of Treg cells10 and alveolar macrophages showing a scavenger resolving (FABP4+) phenotype.15 In the presence of an adequate immune response and virus clearance, IL-33 might drive rapid Treg cell-dependent restoration of respiratory tissue homoeostasis, which probably accounts for the mild or asymptomatic forms of COVID-19 seen in most individuals.