PMC:7546716 / 919-1601 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T17","span":{"begin":1,"end":12},"obj":"Body_part"},{"id":"T18","span":{"begin":13,"end":23},"obj":"Body_part"},{"id":"T19","span":{"begin":63,"end":68},"obj":"Body_part"},{"id":"T20","span":{"begin":199,"end":201},"obj":"Body_part"},{"id":"T21","span":{"begin":248,"end":262},"obj":"Body_part"},{"id":"T22","span":{"begin":413,"end":415},"obj":"Body_part"},{"id":"T23","span":{"begin":457,"end":462},"obj":"Body_part"},{"id":"T24","span":{"begin":471,"end":475},"obj":"Body_part"},{"id":"T25","span":{"begin":488,"end":496},"obj":"Body_part"}],"attributes":[{"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"}],"text":" 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 "}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T8","span":{"begin":146,"end":156},"obj":"Disease"},{"id":"T9","span":{"begin":189,"end":197},"obj":"Disease"},{"id":"T10","span":{"begin":217,"end":235},"obj":"Disease"},{"id":"T11","span":{"begin":585,"end":593},"obj":"Disease"},{"id":"T12","span":{"begin":605,"end":652},"obj":"Disease"},{"id":"T13","span":{"begin":605,"end":638},"obj":"Disease"},{"id":"T14","span":{"begin":654,"end":662},"obj":"Disease"}],"attributes":[{"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"}],"text":" 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 "}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T10","span":{"begin":61,"end":68},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T11","span":{"begin":267,"end":277},"obj":"http://purl.obolibrary.org/obo/CL_0000066"},{"id":"T12","span":{"begin":429,"end":432},"obj":"http://purl.obolibrary.org/obo/CLO_0051025"},{"id":"T13","span":{"begin":455,"end":462},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T14","span":{"begin":471,"end":475},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":" 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 "}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T9","span":{"begin":77,"end":86},"obj":"Chemical"},{"id":"T10","span":{"begin":87,"end":97},"obj":"Chemical"},{"id":"T11","span":{"begin":199,"end":201},"obj":"Chemical"},{"id":"T13","span":{"begin":413,"end":415},"obj":"Chemical"}],"attributes":[{"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"}],"text":" 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 "}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T2","span":{"begin":217,"end":235},"obj":"Phenotype"}],"attributes":[{"id":"A2","pred":"hp_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/HP_0002206"}],"text":" 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 "}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T1","span":{"begin":267,"end":300},"obj":"http://purl.obolibrary.org/obo/GO_0001837"}],"text":" 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 "}

{"project":"LitCovid-sentences","denotations":[{"id":"T8","span":{"begin":158,"end":301},"obj":"Sentence"},{"id":"T9","span":{"begin":302,"end":505},"obj":"Sentence"},{"id":"T10","span":{"begin":507,"end":519},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":" 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 "}

{"project":"LitCovid-PubTator","denotations":[{"id":"28","span":{"begin":1,"end":49},"obj":"Gene"},{"id":"29","span":{"begin":199,"end":204},"obj":"Gene"},{"id":"30","span":{"begin":413,"end":418},"obj":"Gene"},{"id":"31","span":{"begin":429,"end":432},"obj":"Gene"},{"id":"32","span":{"begin":420,"end":422},"obj":"Gene"},{"id":"34","span":{"begin":161,"end":169},"obj":"Species"},{"id":"40","span":{"begin":189,"end":197},"obj":"Disease"},{"id":"41","span":{"begin":217,"end":235},"obj":"Disease"},{"id":"70","span":{"begin":605,"end":652},"obj":"Species"},{"id":"71","span":{"begin":654,"end":664},"obj":"Species"},{"id":"73","span":{"begin":585,"end":593},"obj":"Disease"}],"attributes":[{"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":"A34","pred":"tao:has_database_id","subj":"34","obj":"Tax:9606"},{"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":"A73","pred":"tao:has_database_id","subj":"73","obj":"MESH:C000657245"}],"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":" 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 "}