PMC:7546716 / 575-1876 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T11","span":{"begin":113,"end":117},"obj":"Body_part"},{"id":"T12","span":{"begin":172,"end":174},"obj":"Body_part"},{"id":"T13","span":{"begin":216,"end":221},"obj":"Body_part"},{"id":"T14","span":{"begin":248,"end":253},"obj":"Body_part"},{"id":"T15","span":{"begin":285,"end":287},"obj":"Body_part"},{"id":"T16","span":{"begin":295,"end":299},"obj":"Body_part"},{"id":"T17","span":{"begin":345,"end":356},"obj":"Body_part"},{"id":"T18","span":{"begin":357,"end":367},"obj":"Body_part"},{"id":"T19","span":{"begin":407,"end":412},"obj":"Body_part"},{"id":"T20","span":{"begin":543,"end":545},"obj":"Body_part"},{"id":"T21","span":{"begin":592,"end":606},"obj":"Body_part"},{"id":"T22","span":{"begin":757,"end":759},"obj":"Body_part"},{"id":"T23","span":{"begin":801,"end":806},"obj":"Body_part"},{"id":"T24","span":{"begin":815,"end":819},"obj":"Body_part"},{"id":"T25","span":{"begin":832,"end":840},"obj":"Body_part"},{"id":"T26","span":{"begin":1141,"end":1145},"obj":"Body_part"}],"attributes":[{"id":"A11","pred":"fma_id","subj":"T11","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A12","pred":"fma_id","subj":"T12","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A13","pred":"fma_id","subj":"T13","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A14","pred":"fma_id","subj":"T14","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A15","pred":"fma_id","subj":"T15","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A16","pred":"fma_id","subj":"T16","obj":"http://purl.org/sig/ont/fma/fma12520"},{"id":"A17","pred":"fma_id","subj":"T17","obj":"http://purl.org/sig/ont/fma/fma62854"},{"id":"A18","pred":"fma_id","subj":"T18","obj":"http://purl.org/sig/ont/fma/fma63261"},{"id":"A19","pred":"fma_id","subj":"T19","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A20","pred":"fma_id","subj":"T20","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A21","pred":"fma_id","subj":"T21","obj":"http://purl.org/sig/ont/fma/fma0326458"},{"id":"A22","pred":"fma_id","subj":"T22","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A23","pred":"fma_id","subj":"T23","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A24","pred":"fma_id","subj":"T24","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A25","pred":"fma_id","subj":"T25","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A26","pred":"fma_id","subj":"T26","obj":"http://purl.org/sig/ont/fma/fma7195"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T2","span":{"begin":113,"end":117},"obj":"Body_part"},{"id":"T3","span":{"begin":1141,"end":1145},"obj":"Body_part"}],"attributes":[{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T4","span":{"begin":40,"end":87},"obj":"Disease"},{"id":"T5","span":{"begin":40,"end":73},"obj":"Disease"},{"id":"T6","span":{"begin":113,"end":125},"obj":"Disease"},{"id":"T7","span":{"begin":265,"end":273},"obj":"Disease"},{"id":"T8","span":{"begin":490,"end":500},"obj":"Disease"},{"id":"T9","span":{"begin":533,"end":541},"obj":"Disease"},{"id":"T10","span":{"begin":561,"end":579},"obj":"Disease"},{"id":"T11","span":{"begin":929,"end":937},"obj":"Disease"},{"id":"T12","span":{"begin":949,"end":996},"obj":"Disease"},{"id":"T13","span":{"begin":949,"end":982},"obj":"Disease"},{"id":"T14","span":{"begin":998,"end":1006},"obj":"Disease"},{"id":"T15","span":{"begin":1141,"end":1153},"obj":"Disease"},{"id":"T16","span":{"begin":1170,"end":1178},"obj":"Disease"},{"id":"T17","span":{"begin":1217,"end":1225},"obj":"Disease"},{"id":"T18","span":{"begin":1245,"end":1257},"obj":"Disease"}],"attributes":[{"id":"A4","pred":"mondo_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/MONDO_0005275"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/MONDO_0000831"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/MONDO_0002771"},{"id":"A11","pred":"mondo_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A12","pred":"mondo_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A13","pred":"mondo_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A14","pred":"mondo_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A15","pred":"mondo_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/MONDO_0005275"},{"id":"A16","pred":"mondo_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A17","pred":"mondo_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A18","pred":"mondo_id","subj":"T18","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T5","span":{"begin":113,"end":117},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T6","span":{"begin":113,"end":117},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T7","span":{"begin":200,"end":221},"obj":"http://purl.obolibrary.org/obo/CL_0001065"},{"id":"T8","span":{"begin":246,"end":253},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T9","span":{"begin":291,"end":294},"obj":"http://purl.obolibrary.org/obo/CLO_0051025"},{"id":"T10","span":{"begin":405,"end":412},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T11","span":{"begin":611,"end":621},"obj":"http://purl.obolibrary.org/obo/CL_0000066"},{"id":"T12","span":{"begin":773,"end":776},"obj":"http://purl.obolibrary.org/obo/CLO_0051025"},{"id":"T13","span":{"begin":799,"end":806},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T14","span":{"begin":815,"end":819},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T15","span":{"begin":1141,"end":1145},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T16","span":{"begin":1141,"end":1145},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T5","span":{"begin":172,"end":174},"obj":"Chemical"},{"id":"T7","span":{"begin":285,"end":287},"obj":"Chemical"},{"id":"T9","span":{"begin":421,"end":430},"obj":"Chemical"},{"id":"T10","span":{"begin":431,"end":441},"obj":"Chemical"},{"id":"T11","span":{"begin":543,"end":545},"obj":"Chemical"},{"id":"T13","span":{"begin":757,"end":759},"obj":"Chemical"},{"id":"T15","span":{"begin":1097,"end":1106},"obj":"Chemical"}],"attributes":[{"id":"A5","pred":"chebi_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A6","pred":"chebi_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A7","pred":"chebi_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A8","pred":"chebi_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A9","pred":"chebi_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A10","pred":"chebi_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/CHEBI_52999"},{"id":"A11","pred":"chebi_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A12","pred":"chebi_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A13","pred":"chebi_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A14","pred":"chebi_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A15","pred":"chebi_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T1","span":{"begin":113,"end":125},"obj":"Phenotype"},{"id":"T2","span":{"begin":561,"end":579},"obj":"Phenotype"},{"id":"T3","span":{"begin":1141,"end":1153},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/HP_0002088"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/HP_0002206"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/HP_0002088"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T1","span":{"begin":611,"end":644},"obj":"http://purl.obolibrary.org/obo/GO_0001837"},{"id":"T2","span":{"begin":1245,"end":1257},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-sentences","denotations":[{"id":"T6","span":{"begin":127,"end":254},"obj":"Sentence"},{"id":"T7","span":{"begin":255,"end":501},"obj":"Sentence"},{"id":"T8","span":{"begin":502,"end":645},"obj":"Sentence"},{"id":"T9","span":{"begin":646,"end":849},"obj":"Sentence"},{"id":"T10","span":{"begin":851,"end":863},"obj":"Sentence"},{"id":"T11","span":{"begin":864,"end":1039},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}

{"project":"LitCovid-PubTator","denotations":[{"id":"26","span":{"begin":172,"end":177},"obj":"Gene"},{"id":"27","span":{"begin":285,"end":290},"obj":"Gene"},{"id":"28","span":{"begin":345,"end":393},"obj":"Gene"},{"id":"29","span":{"begin":543,"end":548},"obj":"Gene"},{"id":"30","span":{"begin":757,"end":762},"obj":"Gene"},{"id":"31","span":{"begin":773,"end":776},"obj":"Gene"},{"id":"32","span":{"begin":764,"end":766},"obj":"Gene"},{"id":"33","span":{"begin":40,"end":87},"obj":"Species"},{"id":"34","span":{"begin":505,"end":513},"obj":"Species"},{"id":"35","span":{"begin":291,"end":294},"obj":"Gene"},{"id":"38","span":{"begin":96,"end":125},"obj":"Disease"},{"id":"39","span":{"begin":265,"end":273},"obj":"Disease"},{"id":"40","span":{"begin":533,"end":541},"obj":"Disease"},{"id":"41","span":{"begin":561,"end":579},"obj":"Disease"},{"id":"70","span":{"begin":949,"end":996},"obj":"Species"},{"id":"71","span":{"begin":998,"end":1008},"obj":"Species"},{"id":"72","span":{"begin":1180,"end":1188},"obj":"Species"},{"id":"73","span":{"begin":929,"end":937},"obj":"Disease"},{"id":"74","span":{"begin":1141,"end":1153},"obj":"Disease"},{"id":"75","span":{"begin":1170,"end":1178},"obj":"Disease"},{"id":"76","span":{"begin":1197,"end":1211},"obj":"Disease"},{"id":"77","span":{"begin":1217,"end":1225},"obj":"Disease"},{"id":"78","span":{"begin":1245,"end":1257},"obj":"Disease"}],"attributes":[{"id":"A26","pred":"tao:has_database_id","subj":"26","obj":"Gene:90865"},{"id":"A27","pred":"tao:has_database_id","subj":"27","obj":"Gene:90865"},{"id":"A28","pred":"tao:has_database_id","subj":"28","obj":"Gene:1437"},{"id":"A29","pred":"tao:has_database_id","subj":"29","obj":"Gene:90865"},{"id":"A30","pred":"tao:has_database_id","subj":"30","obj":"Gene:90865"},{"id":"A31","pred":"tao:has_database_id","subj":"31","obj":"Gene:6761"},{"id":"A32","pred":"tao:has_database_id","subj":"32","obj":"Gene:50512"},{"id":"A33","pred":"tao:has_database_id","subj":"33","obj":"Tax:2697049"},{"id":"A34","pred":"tao:has_database_id","subj":"34","obj":"Tax:9606"},{"id":"A35","pred":"tao:has_database_id","subj":"35","obj":"Gene:17082"},{"id":"A38","pred":"tao:has_database_id","subj":"38","obj":"MESH:D008171"},{"id":"A39","pred":"tao:has_database_id","subj":"39","obj":"MESH:C000657245"},{"id":"A40","pred":"tao:has_database_id","subj":"40","obj":"MESH:C000657245"},{"id":"A41","pred":"tao:has_database_id","subj":"41","obj":"MESH:D011658"},{"id":"A70","pred":"tao:has_database_id","subj":"70","obj":"Tax:2697049"},{"id":"A71","pred":"tao:has_database_id","subj":"71","obj":"Tax:2697049"},{"id":"A72","pred":"tao:has_database_id","subj":"72","obj":"Tax:9606"},{"id":"A73","pred":"tao:has_database_id","subj":"73","obj":"MESH:C000657245"},{"id":"A74","pred":"tao:has_database_id","subj":"74","obj":"MESH:D008171"},{"id":"A75","pred":"tao:has_database_id","subj":"75","obj":"MESH:C000657245"},{"id":"A76","pred":"tao:has_database_id","subj":"76","obj":"MESH:D016638"},{"id":"A77","pred":"tao:has_database_id","subj":"77","obj":"MESH:C000657245"},{"id":"A78","pred":"tao:has_database_id","subj":"78","obj":"MESH:D007249"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 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 distres"}