PMC:7546716 / 186-745 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T4","span":{"begin":62,"end":70},"obj":"Body_part"},{"id":"T5","span":{"begin":72,"end":83},"obj":"Body_part"},{"id":"T6","span":{"begin":85,"end":87},"obj":"Body_part"},{"id":"T7","span":{"begin":253,"end":255},"obj":"Body_part"},{"id":"T8","span":{"begin":296,"end":301},"obj":"Body_part"},{"id":"T9","span":{"begin":361,"end":379},"obj":"Body_part"},{"id":"T10","span":{"begin":374,"end":379},"obj":"Body_part"},{"id":"T11","span":{"begin":502,"end":506},"obj":"Body_part"}],"attributes":[{"id":"A4","pred":"fma_id","subj":"T4","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A5","pred":"fma_id","subj":"T5","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A6","pred":"fma_id","subj":"T6","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A7","pred":"fma_id","subj":"T7","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A8","pred":"fma_id","subj":"T8","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A9","pred":"fma_id","subj":"T9","obj":"http://purl.org/sig/ont/fma/fma84070"},{"id":"A10","pred":"fma_id","subj":"T10","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A11","pred":"fma_id","subj":"T11","obj":"http://purl.org/sig/ont/fma/fma7195"}],"text":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T2","span":{"begin":502,"end":506},"obj":"Body_part"}],"attributes":[{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T3","span":{"begin":134,"end":142},"obj":"Disease"},{"id":"T4","span":{"begin":429,"end":476},"obj":"Disease"},{"id":"T5","span":{"begin":429,"end":462},"obj":"Disease"},{"id":"T6","span":{"begin":502,"end":514},"obj":"Disease"}],"attributes":[{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"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"}],"text":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T1","span":{"begin":22,"end":23},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T2","span":{"begin":96,"end":97},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T3","span":{"begin":296,"end":301},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T4","span":{"begin":361,"end":379},"obj":"http://purl.obolibrary.org/obo/CL_0000815"},{"id":"T5","span":{"begin":502,"end":506},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T6","span":{"begin":502,"end":506},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"}],"text":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T1","span":{"begin":85,"end":87},"obj":"Chemical"},{"id":"T3","span":{"begin":253,"end":255},"obj":"Chemical"}],"attributes":[{"id":"A1","pred":"chebi_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A2","pred":"chebi_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A3","pred":"chebi_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A4","pred":"chebi_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"}],"text":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T1","span":{"begin":502,"end":514},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/HP_0002088"}],"text":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}

{"project":"LitCovid-sentences","denotations":[{"id":"T4","span":{"begin":5,"end":224},"obj":"Sentence"},{"id":"T5","span":{"begin":225,"end":515},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}

{"project":"LitCovid-PubTator","denotations":[{"id":"23","span":{"begin":72,"end":91},"obj":"Gene"},{"id":"24","span":{"begin":253,"end":258},"obj":"Gene"},{"id":"25","span":{"begin":328,"end":349},"obj":"Gene"},{"id":"33","span":{"begin":429,"end":476},"obj":"Species"},{"id":"37","span":{"begin":134,"end":142},"obj":"Disease"},{"id":"38","span":{"begin":485,"end":514},"obj":"Disease"}],"attributes":[{"id":"A23","pred":"tao:has_database_id","subj":"23","obj":"Gene:90865"},{"id":"A24","pred":"tao:has_database_id","subj":"24","obj":"Gene:90865"},{"id":"A25","pred":"tao:has_database_id","subj":"25","obj":"Gene:2625"},{"id":"A33","pred":"tao:has_database_id","subj":"33","obj":"Tax:2697049"},{"id":"A37","pred":"tao:has_database_id","subj":"37","obj":"MESH:C000657245"},{"id":"A38","pred":"tao:has_database_id","subj":"38","obj":"MESH:D008171"}],"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":"ies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained b"}