English: Hypothetical mechanisms underlying the cytokine storm induced by SARS-CoV-2 in infected lungs. SARS-CoV-2 enters target cells (e.g. alveolar epithelial cells) via interaction with the ACE2 receptor, thus triggering a complex immune response characterised by activation of pathogenic Th1 cells, CD14+ CD16+ monocytes, alveolar macrophages and Th17 lymphocytes. These cells release high amounts of cytokines and chemokines, responsible for the cytokine storm sustaining a ‘hyperinflammatory’ environment featured by lung infiltration with neutrophils and macrophages. In critically ill COVID-19 patients with ARDS, the Th1-driven immune adaptive response leading to viral clearance appears to be defective (dashed lines). ACE2, angiotensin-converting enzyme 2; APC, antigen presenting cells; ARDS, acute respiratory distress syndrome; COVID-19; coronavirus disease 2019; GM-CSF, granulocyte macrophage-colony stimulating factor; IFN, interferon; IL, interleukin; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; Th, T helper.