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LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T7","span":{"begin":661,"end":665},"obj":"Body_part"},{"id":"T8","span":{"begin":976,"end":980},"obj":"Body_part"},{"id":"T9","span":{"begin":1615,"end":1619},"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"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"IL-33 and cellular drivers of mild–moderate COVID-19\nIn 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.\nBoth ILC2 and γδ T cells are centrally involved in lung homoeostasis and are rapidly activated in response to pathogens including viruses;19, 21 in COVID-19, IL-4 is upregulated at early stages and in milder forms of the disease,10 whereas IL-9 and activated γδ T cells are observed more frequently in mild-to-moderate disease,9, 22 and IFNγ and IL-17 progressively increase with disease severity.6 Vγ9Vδ2+ T cells from patients with COVID-19 have been found to express an effector memory phenotype three times more frequently than do conventional αβ T cells,23 thus suggesting that this T cell subset is selectively stimulated in COVID-19. Because of significantly higher expression of the chemokine receptor CXCR3 compared with their αβ counterparts,24 γδ T cells might be rapidly recruited into inflamed lungs of patients with COVID-19 in response to the observed strong upregulation of the CXCR3 ligands CXCL9 and CXCL10 (figure 1 ).6, 9, 11, 15, 25, 26, 27, 28\nFigure 1 T-cell polarisation in COVID-19\nIL-33 released from virus-damaged cells might induce dysregulated GATA3+Foxp3+ Tregs and promote IL-2 production by dendritic cells, resulting in further expansion of Tregs. IL-33 might also elicit differentiation of ILC2, with TGFβ enhancing ST2 expression on these cells and facilitating production of IL-9. IL-9 in turn stimulates expansion of effector memory Vγ9Vδ2+ T cells with mixed Th1 and Th17 profiles that express CXCR3 and are recruited to the lungs by CXCL9 and CXCL10. IL-9 possibly induces its own transcription factor PU.1 and thus act in an autocrine and paracrine manner (along with TGFβ) to drive proliferation and survival of ILC2 and γδ T cells. Additional positive loops might be fed by IFNγ, which triggers production of CXCL9 and CXCL10 by macrophages. In severe forms of COVID-19, IL-33, along with IL-2 and IL-7 released by dendritic cells, might further stimulate T-cell expansion through STAT5 and induce production of large amounts of GM-CSF by γδ and T helper cells. At advanced stages of disease, aberrant activation of the MyD88-related NF-κB pathway and activation of the NLRP3 inflammasome might induce virus-exposed cells and infiltrating monocytes–macrophages to overproduce IL-1β, IL-23, and IL-6. IL-1β, IL-23, IL-6, and IL-7 act on STAT3 and RORC, thus promoting differentiation of CCR2+ T cells that are recruited to the lungs by CCL2 and CCL8 into γδT17 and Th17 cells producing IL-17 and GM-CSF. In turn, GM-CSF might further recruit and activate proinflammatory monocytes–macrophages. CCR=C-C motif chemokine receptor. CCL=C-C motif chemokine ligand. CXCL=C-X-C motif chemokine ligand. CXCR=C-X-C chemokine receptor. Foxp=forkhead box protein. GATA=GATA-binding factor. GM-CSF=granulocyte-macrophage colony-stimulating factor. IL=interleukin. ILC2=type 2 innate lymphoid cell. MyD88=myeloid differentiation primary response protein. NF-κB=nuclear factor-kappa B. NLRP=NACHT, LRR, and PYD domains-containing protein. PU.1=transcription factor PU.1. RORC=nuclear receptor ROR-gamma. ST2=ST2 receptor. STAT=signal transducer and transcription activator. TGF=transforming growth factor. Th=T-helper. TLR=toll-like receptors. Treg=regulatory T cell."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T8","span":{"begin":138,"end":147},"obj":"Phenotype"},{"id":"T9","span":{"begin":661,"end":673},"obj":"Phenotype"},{"id":"T10","span":{"begin":1553,"end":1562},"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":"IL-33 and cellular drivers of mild–moderate COVID-19\nIn 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.\nBoth ILC2 and γδ T cells are centrally involved in lung homoeostasis and are rapidly activated in response to pathogens including viruses;19, 21 in COVID-19, IL-4 is upregulated at early stages and in milder forms of the disease,10 whereas IL-9 and activated γδ T cells are observed more frequently in mild-to-moderate disease,9, 22 and IFNγ and IL-17 progressively increase with disease severity.6 Vγ9Vδ2+ T cells from patients with COVID-19 have been found to express an effector memory phenotype three times more frequently than do conventional αβ T cells,23 thus suggesting that this T cell subset is selectively stimulated in COVID-19. Because of significantly higher expression of the chemokine receptor CXCR3 compared with their αβ counterparts,24 γδ T cells might be rapidly recruited into inflamed lungs of patients with COVID-19 in response to the observed strong upregulation of the CXCR3 ligands CXCL9 and CXCL10 (figure 1 ).6, 9, 11, 15, 25, 26, 27, 28\nFigure 1 T-cell polarisation in COVID-19\nIL-33 released from virus-damaged cells might induce dysregulated GATA3+Foxp3+ Tregs and promote IL-2 production by dendritic cells, resulting in further expansion of Tregs. IL-33 might also elicit differentiation of ILC2, with TGFβ enhancing ST2 expression on these cells and facilitating production of IL-9. IL-9 in turn stimulates expansion of effector memory Vγ9Vδ2+ T cells with mixed Th1 and Th17 profiles that express CXCR3 and are recruited to the lungs by CXCL9 and CXCL10. IL-9 possibly induces its own transcription factor PU.1 and thus act in an autocrine and paracrine manner (along with TGFβ) to drive proliferation and survival of ILC2 and γδ T cells. Additional positive loops might be fed by IFNγ, which triggers production of CXCL9 and CXCL10 by macrophages. In severe forms of COVID-19, IL-33, along with IL-2 and IL-7 released by dendritic cells, might further stimulate T-cell expansion through STAT5 and induce production of large amounts of GM-CSF by γδ and T helper cells. At advanced stages of disease, aberrant activation of the MyD88-related NF-κB pathway and activation of the NLRP3 inflammasome might induce virus-exposed cells and infiltrating monocytes–macrophages to overproduce IL-1β, IL-23, and IL-6. IL-1β, IL-23, IL-6, and IL-7 act on STAT3 and RORC, thus promoting differentiation of CCR2+ T cells that are recruited to the lungs by CCL2 and CCL8 into γδT17 and Th17 cells producing IL-17 and GM-CSF. In turn, GM-CSF might further recruit and activate proinflammatory monocytes–macrophages. CCR=C-C motif chemokine receptor. CCL=C-C motif chemokine ligand. CXCL=C-X-C motif chemokine ligand. CXCR=C-X-C chemokine receptor. Foxp=forkhead box protein. GATA=GATA-binding factor. GM-CSF=granulocyte-macrophage colony-stimulating factor. IL=interleukin. ILC2=type 2 innate lymphoid cell. MyD88=myeloid differentiation primary response protein. NF-κB=nuclear factor-kappa B. NLRP=NACHT, LRR, and PYD domains-containing protein. PU.1=transcription factor PU.1. RORC=nuclear receptor ROR-gamma. ST2=ST2 receptor. STAT=signal transducer and transcription activator. TGF=transforming growth factor. Th=T-helper. TLR=toll-like receptors. Treg=regulatory T cell."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T10","span":{"begin":383,"end":403},"obj":"http://purl.obolibrary.org/obo/GO_0000981"},{"id":"T11","span":{"begin":383,"end":396},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T12","span":{"begin":598,"end":607},"obj":"http://purl.obolibrary.org/obo/GO_0046903"},{"id":"T13","span":{"begin":981,"end":993},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T14","span":{"begin":1203,"end":1209},"obj":"http://purl.obolibrary.org/obo/GO_0007613"},{"id":"T15","span":{"begin":2046,"end":2052},"obj":"http://purl.obolibrary.org/obo/GO_0007613"},{"id":"T16","span":{"begin":2668,"end":2683},"obj":"http://purl.obolibrary.org/obo/GO_0032623"},{"id":"T17","span":{"begin":2927,"end":2933},"obj":"http://purl.obolibrary.org/obo/GO_0007613"},{"id":"T18","span":{"begin":3084,"end":3104},"obj":"http://purl.obolibrary.org/obo/GO_0000981"},{"id":"T19","span":{"begin":3084,"end":3097},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T20","span":{"begin":3464,"end":3478},"obj":"http://purl.obolibrary.org/obo/GO_0016049"},{"id":"T21","span":{"begin":4535,"end":4555},"obj":"http://purl.obolibrary.org/obo/GO_0000981"},{"id":"T22","span":{"begin":4535,"end":4548},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T23","span":{"begin":4640,"end":4653},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T24","span":{"begin":4682,"end":4688},"obj":"http://purl.obolibrary.org/obo/GO_0040007"}],"text":"IL-33 and cellular drivers of mild–moderate COVID-19\nIn 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.\nBoth ILC2 and γδ T cells are centrally involved in lung homoeostasis and are rapidly activated in response to pathogens including viruses;19, 21 in COVID-19, IL-4 is upregulated at early stages and in milder forms of the disease,10 whereas IL-9 and activated γδ T cells are observed more frequently in mild-to-moderate disease,9, 22 and IFNγ and IL-17 progressively increase with disease severity.6 Vγ9Vδ2+ T cells from patients with COVID-19 have been found to express an effector memory phenotype three times more frequently than do conventional αβ T cells,23 thus suggesting that this T cell subset is selectively stimulated in COVID-19. Because of significantly higher expression of the chemokine receptor CXCR3 compared with their αβ counterparts,24 γδ T cells might be rapidly recruited into inflamed lungs of patients with COVID-19 in response to the observed strong upregulation of the CXCR3 ligands CXCL9 and CXCL10 (figure 1 ).6, 9, 11, 15, 25, 26, 27, 28\nFigure 1 T-cell polarisation in COVID-19\nIL-33 released from virus-damaged cells might induce dysregulated GATA3+Foxp3+ Tregs and promote IL-2 production by dendritic cells, resulting in further expansion of Tregs. IL-33 might also elicit differentiation of ILC2, with TGFβ enhancing ST2 expression on these cells and facilitating production of IL-9. IL-9 in turn stimulates expansion of effector memory Vγ9Vδ2+ T cells with mixed Th1 and Th17 profiles that express CXCR3 and are recruited to the lungs by CXCL9 and CXCL10. IL-9 possibly induces its own transcription factor PU.1 and thus act in an autocrine and paracrine manner (along with TGFβ) to drive proliferation and survival of ILC2 and γδ T cells. Additional positive loops might be fed by IFNγ, which triggers production of CXCL9 and CXCL10 by macrophages. In severe forms of COVID-19, IL-33, along with IL-2 and IL-7 released by dendritic cells, might further stimulate T-cell expansion through STAT5 and induce production of large amounts of GM-CSF by γδ and T helper cells. At advanced stages of disease, aberrant activation of the MyD88-related NF-κB pathway and activation of the NLRP3 inflammasome might induce virus-exposed cells and infiltrating monocytes–macrophages to overproduce IL-1β, IL-23, and IL-6. IL-1β, IL-23, IL-6, and IL-7 act on STAT3 and RORC, thus promoting differentiation of CCR2+ T cells that are recruited to the lungs by CCL2 and CCL8 into γδT17 and Th17 cells producing IL-17 and GM-CSF. In turn, GM-CSF might further recruit and activate proinflammatory monocytes–macrophages. CCR=C-C motif chemokine receptor. CCL=C-C motif chemokine ligand. CXCL=C-X-C motif chemokine ligand. CXCR=C-X-C chemokine receptor. Foxp=forkhead box protein. GATA=GATA-binding factor. GM-CSF=granulocyte-macrophage colony-stimulating factor. IL=interleukin. ILC2=type 2 innate lymphoid cell. MyD88=myeloid differentiation primary response protein. NF-κB=nuclear factor-kappa B. NLRP=NACHT, LRR, and PYD domains-containing protein. PU.1=transcription factor PU.1. RORC=nuclear receptor ROR-gamma. ST2=ST2 receptor. STAT=signal transducer and transcription activator. TGF=transforming growth factor. Th=T-helper. TLR=toll-like receptors. Treg=regulatory T cell."}

LitCovid-sentences

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"33073244-28196763-66244519","span":{"begin":674,"end":676},"obj":"28196763"},{"id":"33073244-32228226-66244520","span":{"begin":770,"end":772},"obj":"32228226"},{"id":"33073244-31911623-66244521","span":{"begin":948,"end":950},"obj":"31911623"},{"id":"33073244-26129648-66244522","span":{"begin":1087,"end":1089},"obj":"26129648"},{"id":"33073244-27543964-66244523","span":{"begin":1091,"end":1093},"obj":"27543964"},{"id":"33073244-27543964-66244524","span":{"begin":1270,"end":1272},"obj":"27543964"},{"id":"33073244-27791087-66244525","span":{"begin":1350,"end":1352},"obj":"27791087"},{"id":"33073244-27543964-66244526","span":{"begin":1702,"end":1704},"obj":"27543964"},{"id":"33073244-28555812-66244527","span":{"begin":1706,"end":1708},"obj":"28555812"},{"id":"33073244-32460357-66244528","span":{"begin":1793,"end":1795},"obj":"32460357"},{"id":"33073244-31986264-66244529","span":{"begin":1891,"end":1892},"obj":"31986264"},{"id":"33073244-32467616-66244530","span":{"begin":2123,"end":2125},"obj":"32467616"},{"id":"33073244-11994442-66244531","span":{"begin":2316,"end":2318},"obj":"11994442"},{"id":"33073244-31986264-66244532","span":{"begin":2504,"end":2505},"obj":"31986264"},{"id":"33073244-32228226-66244533","span":{"begin":2507,"end":2509},"obj":"32228226"},{"id":"33073244-32398875-66244534","span":{"begin":2511,"end":2513},"obj":"32398875"},{"id":"33073244-32360286-66244535","span":{"begin":2515,"end":2517},"obj":"32360286"},{"id":"33073244-32407669-66244536","span":{"begin":2519,"end":2521},"obj":"32407669"},{"id":"33073244-32416070-66244537","span":{"begin":2523,"end":2525},"obj":"32416070"}],"text":"IL-33 and cellular drivers of mild–moderate COVID-19\nIn 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.\nBoth ILC2 and γδ T cells are centrally involved in lung homoeostasis and are rapidly activated in response to pathogens including viruses;19, 21 in COVID-19, IL-4 is upregulated at early stages and in milder forms of the disease,10 whereas IL-9 and activated γδ T cells are observed more frequently in mild-to-moderate disease,9, 22 and IFNγ and IL-17 progressively increase with disease severity.6 Vγ9Vδ2+ T cells from patients with COVID-19 have been found to express an effector memory phenotype three times more frequently than do conventional αβ T cells,23 thus suggesting that this T cell subset is selectively stimulated in COVID-19. Because of significantly higher expression of the chemokine receptor CXCR3 compared with their αβ counterparts,24 γδ T cells might be rapidly recruited into inflamed lungs of patients with COVID-19 in response to the observed strong upregulation of the CXCR3 ligands CXCL9 and CXCL10 (figure 1 ).6, 9, 11, 15, 25, 26, 27, 28\nFigure 1 T-cell polarisation in COVID-19\nIL-33 released from virus-damaged cells might induce dysregulated GATA3+Foxp3+ Tregs and promote IL-2 production by dendritic cells, resulting in further expansion of Tregs. IL-33 might also elicit differentiation of ILC2, with TGFβ enhancing ST2 expression on these cells and facilitating production of IL-9. IL-9 in turn stimulates expansion of effector memory Vγ9Vδ2+ T cells with mixed Th1 and Th17 profiles that express CXCR3 and are recruited to the lungs by CXCL9 and CXCL10. IL-9 possibly induces its own transcription factor PU.1 and thus act in an autocrine and paracrine manner (along with TGFβ) to drive proliferation and survival of ILC2 and γδ T cells. Additional positive loops might be fed by IFNγ, which triggers production of CXCL9 and CXCL10 by macrophages. In severe forms of COVID-19, IL-33, along with IL-2 and IL-7 released by dendritic cells, might further stimulate T-cell expansion through STAT5 and induce production of large amounts of GM-CSF by γδ and T helper cells. At advanced stages of disease, aberrant activation of the MyD88-related NF-κB pathway and activation of the NLRP3 inflammasome might induce virus-exposed cells and infiltrating monocytes–macrophages to overproduce IL-1β, IL-23, and IL-6. IL-1β, IL-23, IL-6, and IL-7 act on STAT3 and RORC, thus promoting differentiation of CCR2+ T cells that are recruited to the lungs by CCL2 and CCL8 into γδT17 and Th17 cells producing IL-17 and GM-CSF. In turn, GM-CSF might further recruit and activate proinflammatory monocytes–macrophages. CCR=C-C motif chemokine receptor. CCL=C-C motif chemokine ligand. CXCL=C-X-C motif chemokine ligand. CXCR=C-X-C chemokine receptor. Foxp=forkhead box protein. GATA=GATA-binding factor. GM-CSF=granulocyte-macrophage colony-stimulating factor. IL=interleukin. ILC2=type 2 innate lymphoid cell. MyD88=myeloid differentiation primary response protein. NF-κB=nuclear factor-kappa B. NLRP=NACHT, LRR, and PYD domains-containing protein. PU.1=transcription factor PU.1. RORC=nuclear receptor ROR-gamma. ST2=ST2 receptor. STAT=signal transducer and transcription activator. TGF=transforming growth factor. Th=T-helper. TLR=toll-like receptors. Treg=regulatory T cell."}

PMC:7546716 / 4903-9661 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7546716 / 4903-9661 JSON TXT