PMC:7200337 / 26025-27804 JSON TXT

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2_test

{"project":"2_test","denotations":[{"id":"32505227-9486650-46575289","span":{"begin":207,"end":211},"obj":"9486650"},{"id":"32505227-9034158-46575290","span":{"begin":228,"end":232},"obj":"9034158"},{"id":"32505227-29302013-46575291","span":{"begin":334,"end":338},"obj":"29302013"},{"id":"32505227-26251193-46575293","span":{"begin":1033,"end":1037},"obj":"26251193"},{"id":"32505227-19559672-46575295","span":{"begin":1367,"end":1371},"obj":"19559672"},{"id":"32505227-30524877-46575296","span":{"begin":1430,"end":1434},"obj":"30524877"},{"id":"T58402","span":{"begin":207,"end":211},"obj":"9486650"},{"id":"T11232","span":{"begin":228,"end":232},"obj":"9034158"},{"id":"T15390","span":{"begin":334,"end":338},"obj":"29302013"},{"id":"T84673","span":{"begin":1033,"end":1037},"obj":"26251193"},{"id":"T83308","span":{"begin":1367,"end":1371},"obj":"19559672"},{"id":"T78837","span":{"begin":1430,"end":1434},"obj":"30524877"}],"text":"The immune checkpoint NKG2A is increased on NK cells and CD8 T cells from COVID-19 patients (Zheng et al., 2020b). NKG2A inhibits cell cytotoxicity by binding the non-classical HLA-E molecule (Braud et al., 1998, Brooks et al., 1997), and this interaction is strongly correlated with poor control of HIV-1 infection (Ramsuran et al., 2018). Genes encoding the inhibitory receptors LAG3 and TIM3 are also upregulated in NK cells from COVID-19 patients (Wilk et al., 2020, Hadjadj et al., 2020). Thus, increased immune checkpoints on NK cells might contribute to viral escape. Additionally, COVID-19 patients have higher plasma concentrations of IL-6 (Huang et al., 2020b), which significantly correlate with lower NK cell numbers (Wang et al., 2020d, Wang et al., 2020f). In vitro stimulation by IL-6 and soluble IL-6 receptor has previously revealed impaired cytolytic functions (perforin and granzyme B production) by healthy donor NK cells, which can be restored following addition of tocilizumab (IL-6R blockade) (Cifaldi et al., 2015). TNF-α is also upregulated in the plasma of COVID-19 patients (Huang et al., 2020b), and ligand-receptor interaction analysis of peripheral blood scRNA-seq data suggests that monocyte-secreted TNF-α might bind to its receptors on NK cells (Guo et al., 2020). TNF-α is known to contribute to NK cell differentiation (Lee et al., 2009), which includes downregulation of NKp46 (Ivagnès et al., 2017), though no effect of TNF-α or IL-6 on NK cell-mediated ADCC has been reported so far. Collectively, these data suggest that crosstalk with monocytes might impair NK cell recognition and killing of SARS-CoV-2-infected cells, and antibodies targeting IL-6 and TNF-signaling may benefit enhanced NK cell functions in COVID-19 patients (Figure 2)."}

LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T28","span":{"begin":1179,"end":1184},"obj":"Body_part"}],"attributes":[{"id":"A28","pred":"uberon_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"The immune checkpoint NKG2A is increased on NK cells and CD8 T cells from COVID-19 patients (Zheng et al., 2020b). NKG2A inhibits cell cytotoxicity by binding the non-classical HLA-E molecule (Braud et al., 1998, Brooks et al., 1997), and this interaction is strongly correlated with poor control of HIV-1 infection (Ramsuran et al., 2018). Genes encoding the inhibitory receptors LAG3 and TIM3 are also upregulated in NK cells from COVID-19 patients (Wilk et al., 2020, Hadjadj et al., 2020). Thus, increased immune checkpoints on NK cells might contribute to viral escape. Additionally, COVID-19 patients have higher plasma concentrations of IL-6 (Huang et al., 2020b), which significantly correlate with lower NK cell numbers (Wang et al., 2020d, Wang et al., 2020f). In vitro stimulation by IL-6 and soluble IL-6 receptor has previously revealed impaired cytolytic functions (perforin and granzyme B production) by healthy donor NK cells, which can be restored following addition of tocilizumab (IL-6R blockade) (Cifaldi et al., 2015). TNF-α is also upregulated in the plasma of COVID-19 patients (Huang et al., 2020b), and ligand-receptor interaction analysis of peripheral blood scRNA-seq data suggests that monocyte-secreted TNF-α might bind to its receptors on NK cells (Guo et al., 2020). TNF-α is known to contribute to NK cell differentiation (Lee et al., 2009), which includes downregulation of NKp46 (Ivagnès et al., 2017), though no effect of TNF-α or IL-6 on NK cell-mediated ADCC has been reported so far. Collectively, these data suggest that crosstalk with monocytes might impair NK cell recognition and killing of SARS-CoV-2-infected cells, and antibodies targeting IL-6 and TNF-signaling may benefit enhanced NK cell functions in COVID-19 patients (Figure 2)."}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T176","span":{"begin":74,"end":82},"obj":"Disease"},{"id":"T177","span":{"begin":306,"end":315},"obj":"Disease"},{"id":"T178","span":{"begin":433,"end":441},"obj":"Disease"},{"id":"T179","span":{"begin":589,"end":597},"obj":"Disease"},{"id":"T180","span":{"begin":1083,"end":1091},"obj":"Disease"},{"id":"T181","span":{"begin":1491,"end":1495},"obj":"Disease"},{"id":"T182","span":{"begin":1633,"end":1641},"obj":"Disease"},{"id":"T183","span":{"begin":1750,"end":1758},"obj":"Disease"}],"attributes":[{"id":"A176","pred":"mondo_id","subj":"T176","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A177","pred":"mondo_id","subj":"T177","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A178","pred":"mondo_id","subj":"T178","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A179","pred":"mondo_id","subj":"T179","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A180","pred":"mondo_id","subj":"T180","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A181","pred":"mondo_id","subj":"T181","obj":"http://purl.obolibrary.org/obo/MONDO_0008734"},{"id":"A182","pred":"mondo_id","subj":"T182","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A183","pred":"mondo_id","subj":"T183","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"The immune checkpoint NKG2A is increased on NK cells and CD8 T cells from COVID-19 patients (Zheng et al., 2020b). NKG2A inhibits cell cytotoxicity by binding the non-classical HLA-E molecule (Braud et al., 1998, Brooks et al., 1997), and this interaction is strongly correlated with poor control of HIV-1 infection (Ramsuran et al., 2018). Genes encoding the inhibitory receptors LAG3 and TIM3 are also upregulated in NK cells from COVID-19 patients (Wilk et al., 2020, Hadjadj et al., 2020). Thus, increased immune checkpoints on NK cells might contribute to viral escape. Additionally, COVID-19 patients have higher plasma concentrations of IL-6 (Huang et al., 2020b), which significantly correlate with lower NK cell numbers (Wang et al., 2020d, Wang et al., 2020f). In vitro stimulation by IL-6 and soluble IL-6 receptor has previously revealed impaired cytolytic functions (perforin and granzyme B production) by healthy donor NK cells, which can be restored following addition of tocilizumab (IL-6R blockade) (Cifaldi et al., 2015). TNF-α is also upregulated in the plasma of COVID-19 patients (Huang et al., 2020b), and ligand-receptor interaction analysis of peripheral blood scRNA-seq data suggests that monocyte-secreted TNF-α might bind to its receptors on NK cells (Guo et al., 2020). TNF-α is known to contribute to NK cell differentiation (Lee et al., 2009), which includes downregulation of NKp46 (Ivagnès et al., 2017), though no effect of TNF-α or IL-6 on NK cell-mediated ADCC has been reported so far. Collectively, these data suggest that crosstalk with monocytes might impair NK cell recognition and killing of SARS-CoV-2-infected cells, and antibodies targeting IL-6 and TNF-signaling may benefit enhanced NK cell functions in COVID-19 patients (Figure 2)."}

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T111","span":{"begin":893,"end":914},"obj":"http://purl.obolibrary.org/obo/GO_0071613"},{"id":"T112","span":{"begin":1000,"end":1005},"obj":"http://purl.obolibrary.org/obo/GO_0004915"},{"id":"T113","span":{"begin":1330,"end":1353},"obj":"http://purl.obolibrary.org/obo/GO_0001779"},{"id":"T114","span":{"begin":1333,"end":1353},"obj":"http://purl.obolibrary.org/obo/GO_0030154"},{"id":"T115","span":{"begin":1491,"end":1495},"obj":"http://purl.obolibrary.org/obo/GO_0001788"},{"id":"T116","span":{"begin":1601,"end":1617},"obj":"http://purl.obolibrary.org/obo/GO_0008037"},{"id":"T117","span":{"begin":1698,"end":1707},"obj":"http://purl.obolibrary.org/obo/GO_0023052"}],"text":"The immune checkpoint NKG2A is increased on NK cells and CD8 T cells from COVID-19 patients (Zheng et al., 2020b). NKG2A inhibits cell cytotoxicity by binding the non-classical HLA-E molecule (Braud et al., 1998, Brooks et al., 1997), and this interaction is strongly correlated with poor control of HIV-1 infection (Ramsuran et al., 2018). Genes encoding the inhibitory receptors LAG3 and TIM3 are also upregulated in NK cells from COVID-19 patients (Wilk et al., 2020, Hadjadj et al., 2020). Thus, increased immune checkpoints on NK cells might contribute to viral escape. Additionally, COVID-19 patients have higher plasma concentrations of IL-6 (Huang et al., 2020b), which significantly correlate with lower NK cell numbers (Wang et al., 2020d, Wang et al., 2020f). In vitro stimulation by IL-6 and soluble IL-6 receptor has previously revealed impaired cytolytic functions (perforin and granzyme B production) by healthy donor NK cells, which can be restored following addition of tocilizumab (IL-6R blockade) (Cifaldi et al., 2015). TNF-α is also upregulated in the plasma of COVID-19 patients (Huang et al., 2020b), and ligand-receptor interaction analysis of peripheral blood scRNA-seq data suggests that monocyte-secreted TNF-α might bind to its receptors on NK cells (Guo et al., 2020). TNF-α is known to contribute to NK cell differentiation (Lee et al., 2009), which includes downregulation of NKp46 (Ivagnès et al., 2017), though no effect of TNF-α or IL-6 on NK cell-mediated ADCC has been reported so far. Collectively, these data suggest that crosstalk with monocytes might impair NK cell recognition and killing of SARS-CoV-2-infected cells, and antibodies targeting IL-6 and TNF-signaling may benefit enhanced NK cell functions in COVID-19 patients (Figure 2)."}

LitCovid-PubTator

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T145","span":{"begin":0,"end":114},"obj":"Sentence"},{"id":"T146","span":{"begin":115,"end":340},"obj":"Sentence"},{"id":"T147","span":{"begin":341,"end":493},"obj":"Sentence"},{"id":"T148","span":{"begin":494,"end":574},"obj":"Sentence"},{"id":"T149","span":{"begin":575,"end":770},"obj":"Sentence"},{"id":"T150","span":{"begin":771,"end":1039},"obj":"Sentence"},{"id":"T151","span":{"begin":1040,"end":1297},"obj":"Sentence"},{"id":"T152","span":{"begin":1298,"end":1521},"obj":"Sentence"},{"id":"T153","span":{"begin":1522,"end":1779},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"The immune checkpoint NKG2A is increased on NK cells and CD8 T cells from COVID-19 patients (Zheng et al., 2020b). NKG2A inhibits cell cytotoxicity by binding the non-classical HLA-E molecule (Braud et al., 1998, Brooks et al., 1997), and this interaction is strongly correlated with poor control of HIV-1 infection (Ramsuran et al., 2018). Genes encoding the inhibitory receptors LAG3 and TIM3 are also upregulated in NK cells from COVID-19 patients (Wilk et al., 2020, Hadjadj et al., 2020). Thus, increased immune checkpoints on NK cells might contribute to viral escape. Additionally, COVID-19 patients have higher plasma concentrations of IL-6 (Huang et al., 2020b), which significantly correlate with lower NK cell numbers (Wang et al., 2020d, Wang et al., 2020f). In vitro stimulation by IL-6 and soluble IL-6 receptor has previously revealed impaired cytolytic functions (perforin and granzyme B production) by healthy donor NK cells, which can be restored following addition of tocilizumab (IL-6R blockade) (Cifaldi et al., 2015). TNF-α is also upregulated in the plasma of COVID-19 patients (Huang et al., 2020b), and ligand-receptor interaction analysis of peripheral blood scRNA-seq data suggests that monocyte-secreted TNF-α might bind to its receptors on NK cells (Guo et al., 2020). TNF-α is known to contribute to NK cell differentiation (Lee et al., 2009), which includes downregulation of NKp46 (Ivagnès et al., 2017), though no effect of TNF-α or IL-6 on NK cell-mediated ADCC has been reported so far. Collectively, these data suggest that crosstalk with monocytes might impair NK cell recognition and killing of SARS-CoV-2-infected cells, and antibodies targeting IL-6 and TNF-signaling may benefit enhanced NK cell functions in COVID-19 patients (Figure 2)."}

PMC:7200337 / 26025-27804 JSONTXT

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PMC:7200337 / 26025-27804 JSON TXT