PMC:7546716 / 746-1284 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T12","span":{"begin":1,"end":3},"obj":"Body_part"},{"id":"T13","span":{"begin":45,"end":50},"obj":"Body_part"},{"id":"T14","span":{"begin":77,"end":82},"obj":"Body_part"},{"id":"T15","span":{"begin":114,"end":116},"obj":"Body_part"},{"id":"T16","span":{"begin":124,"end":128},"obj":"Body_part"},{"id":"T17","span":{"begin":174,"end":185},"obj":"Body_part"},{"id":"T18","span":{"begin":186,"end":196},"obj":"Body_part"},{"id":"T19","span":{"begin":236,"end":241},"obj":"Body_part"},{"id":"T20","span":{"begin":372,"end":374},"obj":"Body_part"},{"id":"T21","span":{"begin":421,"end":435},"obj":"Body_part"}],"attributes":[{"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"}],"text":" 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 p"}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T7","span":{"begin":94,"end":102},"obj":"Disease"},{"id":"T8","span":{"begin":319,"end":329},"obj":"Disease"},{"id":"T9","span":{"begin":362,"end":370},"obj":"Disease"},{"id":"T10","span":{"begin":390,"end":408},"obj":"Disease"}],"attributes":[{"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"}],"text":" 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 p"}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T7","span":{"begin":29,"end":50},"obj":"http://purl.obolibrary.org/obo/CL_0001065"},{"id":"T8","span":{"begin":75,"end":82},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T9","span":{"begin":120,"end":123},"obj":"http://purl.obolibrary.org/obo/CLO_0051025"},{"id":"T10","span":{"begin":234,"end":241},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T11","span":{"begin":440,"end":450},"obj":"http://purl.obolibrary.org/obo/CL_0000066"}],"text":" 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 p"}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T5","span":{"begin":1,"end":3},"obj":"Chemical"},{"id":"T7","span":{"begin":114,"end":116},"obj":"Chemical"},{"id":"T9","span":{"begin":250,"end":259},"obj":"Chemical"},{"id":"T10","span":{"begin":260,"end":270},"obj":"Chemical"},{"id":"T11","span":{"begin":372,"end":374},"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"}],"text":" 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 p"}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T2","span":{"begin":390,"end":408},"obj":"Phenotype"}],"attributes":[{"id":"A2","pred":"hp_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/HP_0002206"}],"text":" 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 p"}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T1","span":{"begin":440,"end":473},"obj":"http://purl.obolibrary.org/obo/GO_0001837"}],"text":" 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 p"}

{"project":"LitCovid-sentences","denotations":[{"id":"T7","span":{"begin":84,"end":330},"obj":"Sentence"},{"id":"T8","span":{"begin":331,"end":474},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":" 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 p"}

{"project":"LitCovid-PubTator","denotations":[{"id":"26","span":{"begin":1,"end":6},"obj":"Gene"},{"id":"27","span":{"begin":114,"end":119},"obj":"Gene"},{"id":"28","span":{"begin":174,"end":222},"obj":"Gene"},{"id":"29","span":{"begin":372,"end":377},"obj":"Gene"},{"id":"34","span":{"begin":334,"end":342},"obj":"Species"},{"id":"35","span":{"begin":120,"end":123},"obj":"Gene"},{"id":"39","span":{"begin":94,"end":102},"obj":"Disease"},{"id":"40","span":{"begin":362,"end":370},"obj":"Disease"},{"id":"41","span":{"begin":390,"end":408},"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":"A34","pred":"tao:has_database_id","subj":"34","obj":"Tax:9606"},{"id":"A35","pred":"tao:has_database_id","subj":"35","obj":"Gene:17082"},{"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"}],"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":" 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 p"}