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LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T7","span":{"begin":608,"end":612},"obj":"Body_part"},{"id":"T8","span":{"begin":923,"end":927},"obj":"Body_part"}],"attributes":[{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"In susceptible individuals who develop symptomatic SARS-CoV-2 infection and COVID-19 pneumonia (eg, in the presence of individual cytokine or receptor polymorphisms), IL-33 might abnormally upregulate expression of its own receptor ST2 (also known as IL-1RL1) on Treg cells, resulting in increased expression of the canonical Th2 transcription factor GATA-binding factor 3 (GATA3), which impairs the suppressive function of Treg cells. The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of pneumonia."}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T49","span":{"begin":51,"end":59},"obj":"Disease"},{"id":"T50","span":{"begin":62,"end":71},"obj":"Disease"},{"id":"T51","span":{"begin":76,"end":84},"obj":"Disease"},{"id":"T52","span":{"begin":85,"end":94},"obj":"Disease"},{"id":"T53","span":{"begin":608,"end":620},"obj":"Disease"},{"id":"T54","span":{"begin":928,"end":940},"obj":"Disease"},{"id":"T55","span":{"begin":1451,"end":1459},"obj":"Disease"},{"id":"T56","span":{"begin":1500,"end":1509},"obj":"Disease"}],"attributes":[{"id":"A49","pred":"mondo_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A50","pred":"mondo_id","subj":"T50","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A51","pred":"mondo_id","subj":"T51","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A52","pred":"mondo_id","subj":"T52","obj":"http://purl.obolibrary.org/obo/MONDO_0005249"},{"id":"A53","pred":"mondo_id","subj":"T53","obj":"http://purl.obolibrary.org/obo/MONDO_0005275"},{"id":"A54","pred":"mondo_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A55","pred":"mondo_id","subj":"T55","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A56","pred":"mondo_id","subj":"T56","obj":"http://purl.obolibrary.org/obo/MONDO_0005249"}],"text":"In susceptible individuals who develop symptomatic SARS-CoV-2 infection and COVID-19 pneumonia (eg, in the presence of individual cytokine or receptor polymorphisms), IL-33 might abnormally upregulate expression of its own receptor ST2 (also known as IL-1RL1) on Treg cells, resulting in increased expression of the canonical Th2 transcription factor GATA-binding factor 3 (GATA3), which impairs the suppressive function of Treg cells. The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of pneumonia."}

LitCovid-PD-CLO

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T54","span":{"begin":167,"end":169},"obj":"Chemical"},{"id":"T56","span":{"begin":251,"end":253},"obj":"Chemical"},{"id":"T58","span":{"begin":787,"end":789},"obj":"Chemical"},{"id":"T60","span":{"begin":971,"end":973},"obj":"Chemical"},{"id":"T62","span":{"begin":1041,"end":1043},"obj":"Chemical"},{"id":"T64","span":{"begin":1141,"end":1149},"obj":"Chemical"},{"id":"T65","span":{"begin":1292,"end":1294},"obj":"Chemical"},{"id":"T67","span":{"begin":1351,"end":1353},"obj":"Chemical"},{"id":"T69","span":{"begin":1365,"end":1367},"obj":"Chemical"}],"attributes":[{"id":"A54","pred":"chebi_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A55","pred":"chebi_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A56","pred":"chebi_id","subj":"T56","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A57","pred":"chebi_id","subj":"T56","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A58","pred":"chebi_id","subj":"T58","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A59","pred":"chebi_id","subj":"T58","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A60","pred":"chebi_id","subj":"T60","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A61","pred":"chebi_id","subj":"T60","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A62","pred":"chebi_id","subj":"T62","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A63","pred":"chebi_id","subj":"T62","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A64","pred":"chebi_id","subj":"T64","obj":"http://purl.obolibrary.org/obo/CHEBI_35224"},{"id":"A65","pred":"chebi_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A66","pred":"chebi_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A67","pred":"chebi_id","subj":"T67","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A68","pred":"chebi_id","subj":"T67","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A69","pred":"chebi_id","subj":"T69","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A70","pred":"chebi_id","subj":"T69","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"}],"text":"In susceptible individuals who develop symptomatic SARS-CoV-2 infection and COVID-19 pneumonia (eg, in the presence of individual cytokine or receptor polymorphisms), IL-33 might abnormally upregulate expression of its own receptor ST2 (also known as IL-1RL1) on Treg cells, resulting in increased expression of the canonical Th2 transcription factor GATA-binding factor 3 (GATA3), which impairs the suppressive function of Treg cells. The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of pneumonia."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T8","span":{"begin":85,"end":94},"obj":"Phenotype"},{"id":"T9","span":{"begin":608,"end":620},"obj":"Phenotype"},{"id":"T10","span":{"begin":1500,"end":1509},"obj":"Phenotype"}],"attributes":[{"id":"A8","pred":"hp_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/HP_0002090"},{"id":"A9","pred":"hp_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/HP_0002088"},{"id":"A10","pred":"hp_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/HP_0002090"}],"text":"In susceptible individuals who develop symptomatic SARS-CoV-2 infection and COVID-19 pneumonia (eg, in the presence of individual cytokine or receptor polymorphisms), IL-33 might abnormally upregulate expression of its own receptor ST2 (also known as IL-1RL1) on Treg cells, resulting in increased expression of the canonical Th2 transcription factor GATA-binding factor 3 (GATA3), which impairs the suppressive function of Treg cells. The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of pneumonia."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T10","span":{"begin":330,"end":350},"obj":"http://purl.obolibrary.org/obo/GO_0000981"},{"id":"T11","span":{"begin":330,"end":343},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T12","span":{"begin":545,"end":554},"obj":"http://purl.obolibrary.org/obo/GO_0046903"},{"id":"T13","span":{"begin":928,"end":940},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T14","span":{"begin":1150,"end":1156},"obj":"http://purl.obolibrary.org/obo/GO_0007613"}],"text":"In susceptible individuals who develop symptomatic SARS-CoV-2 infection and COVID-19 pneumonia (eg, in the presence of individual cytokine or receptor polymorphisms), IL-33 might abnormally upregulate expression of its own receptor ST2 (also known as IL-1RL1) on Treg cells, resulting in increased expression of the canonical Th2 transcription factor GATA-binding factor 3 (GATA3), which impairs the suppressive function of Treg cells. The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of pneumonia."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T20","span":{"begin":0,"end":435},"obj":"Sentence"},{"id":"T21","span":{"begin":436,"end":1510},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"In susceptible individuals who develop symptomatic SARS-CoV-2 infection and COVID-19 pneumonia (eg, in the presence of individual cytokine or receptor polymorphisms), IL-33 might abnormally upregulate expression of its own receptor ST2 (also known as IL-1RL1) on Treg cells, resulting in increased expression of the canonical Th2 transcription factor GATA-binding factor 3 (GATA3), which impairs the suppressive function of Treg cells. The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of pneumonia."}

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"33073244-28196763-66244519","span":{"begin":621,"end":623},"obj":"28196763"},{"id":"33073244-32228226-66244520","span":{"begin":717,"end":719},"obj":"32228226"},{"id":"33073244-31911623-66244521","span":{"begin":895,"end":897},"obj":"31911623"},{"id":"33073244-26129648-66244522","span":{"begin":1034,"end":1036},"obj":"26129648"},{"id":"33073244-27543964-66244523","span":{"begin":1038,"end":1040},"obj":"27543964"},{"id":"33073244-27543964-66244524","span":{"begin":1217,"end":1219},"obj":"27543964"},{"id":"33073244-27791087-66244525","span":{"begin":1297,"end":1299},"obj":"27791087"}],"text":"In susceptible individuals who develop symptomatic SARS-CoV-2 infection and COVID-19 pneumonia (eg, in the presence of individual cytokine or receptor polymorphisms), IL-33 might abnormally upregulate expression of its own receptor ST2 (also known as IL-1RL1) on Treg cells, resulting in increased expression of the canonical Th2 transcription factor GATA-binding factor 3 (GATA3), which impairs the suppressive function of Treg cells. The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of pneumonia."}

PMC:7546716 / 4956-6466 JSONTXT

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PMC:7546716 / 4956-6466 JSON TXT