PMC:7546716 / 868-2160 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7546716","sourcedb":"PMC","sourceid":"7546716","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7546716","text":"2 axis might act to expand the number of pathogenic granulocyte–macrophage colony-stimulating factor-expressing T cells, dampen antiviral interferon responses, elicit hyperinflammation, and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target IL-33 (eg, anti-ST2), T helper 17-like γδ T cells, immune cell homing, and cytokine balance.\n\nIntroduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as 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