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LitCovid-PD-FMA-UBERON

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T37","span":{"begin":373,"end":389},"obj":"Disease"},{"id":"T38","span":{"begin":1237,"end":1249},"obj":"Disease"},{"id":"T39","span":{"begin":1443,"end":1455},"obj":"Disease"},{"id":"T40","span":{"begin":2529,"end":2533},"obj":"Disease"}],"attributes":[{"id":"A37","pred":"mondo_id","subj":"T37","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A38","pred":"mondo_id","subj":"T38","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A39","pred":"mondo_id","subj":"T39","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A40","pred":"mondo_id","subj":"T40","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"}],"text":"The binding of the cytokine to its transmembrane cell surface receptor activates an intracellular signal transduction pathway, generally a Janus kinase (Jak), which, via a kinase cascade, phosphorylates its transcription protein (STAT). Phosphorylated STAT dimers and moves to the nucleus, initiating a new gene transcription. Mutation of STAT1 increases susceptibility to virus infections because it is involved in various signalling pathways, including IFN-α/β, IFN- γ, IFN-l, IL-2, IL-3, IL-6, IL-9, IL-10, IL-11, IL-12, IL-15, IL-21, IL-22, IL-26 and IL-27 [10], and chemokines of several types such as C-X-C motif chemokine ligand 10 (CXCL-10), Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES)/Chemokine (C–C motif) ligand 5 (CCL-5), Monocyte Chemoattractant Protein-1 (MCP-1) [11]. IFN-γ promotes antigen-specific antibody production, increasing the activity of phagocytosis. In the meantime, PRRs trigger inflammatory signalling, with activation of transcription factors like nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB). NFκB is the key transcriptional regulator of many pro-inflammatory cytokines, adhesion molecules, chemokines, growth factors and other mediators of inflammation, as tumour necrosis factor (TNF), interleukins 1 (IL-1β), 6 (IL-6), and 12 (IL-12), promotes cellular proliferation and protects against apoptosis providing a mechanism that determines chronic inflammation. The recognition of pathogens is achieved through the presence of pattern recognition receptors (PRRs) [12]. PRRs identify the microbe-associated molecular patterns (MAMPs), and defensive responses is activated. PRRs include Toll-like receptors (TLRs), that are able to recognize viral DNA, viral double-stranded RNA and viral single-stranded RNA. TLRs are expressed on macrophages, dendritic cells, neutrophils, eosinophils, epithelial cells and keratinocytes. In particular, intracellular TLR-7 and TLR-8 allow the innate recognition of the single-stranded RNA of coronaviruses [13]. Intracellular and extracellular PRRs recognized spike glycoprotein, of the coronavirus coat, starting the inflammatory process, through the NFκB pathway [14]. Moreover, Nucleotide-Binding Domain, Leucine-Rich Repeat (NLR) proteins have also been identified, and NALP3 (NACHT, LRR and PYD domains-containing protein 3) has a special function in the innate immune response [15]. The processes involved in antiviral immunity is shown in Fig. 1.\nFig. 1 Graphical representation of antiviral SARS-Coronavirus 2 immunity. B: B lymphocyte; CTL: cytotoxic; T lymphocyte; IFN: interferon; Ig: immunoglobulin; IL: interleukin; MHC: major histocompatibility class; NFκB: nuclear factor kappa-light- chain- enhancer of activated B cells; NK: natural killer cell; Th: helper T lymphocyte; TLR: Toll-like receptor; TNF: tumour necrosis factor"}

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T8","span":{"begin":1254,"end":1260},"obj":"Phenotype"},{"id":"T9","span":{"begin":2848,"end":2854},"obj":"Phenotype"}],"attributes":[{"id":"A8","pred":"hp_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/HP_0002664"},{"id":"A9","pred":"hp_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/HP_0002664"}],"text":"The binding of the cytokine to its transmembrane cell surface receptor activates an intracellular signal transduction pathway, generally a Janus kinase (Jak), which, via a kinase cascade, phosphorylates its transcription protein (STAT). Phosphorylated STAT dimers and moves to the nucleus, initiating a new gene transcription. Mutation of STAT1 increases susceptibility to virus infections because it is involved in various signalling pathways, including IFN-α/β, IFN- γ, IFN-l, IL-2, IL-3, IL-6, IL-9, IL-10, IL-11, IL-12, IL-15, IL-21, IL-22, IL-26 and IL-27 [10], and chemokines of several types such as C-X-C motif chemokine ligand 10 (CXCL-10), Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES)/Chemokine (C–C motif) ligand 5 (CCL-5), Monocyte Chemoattractant Protein-1 (MCP-1) [11]. IFN-γ promotes antigen-specific antibody production, increasing the activity of phagocytosis. In the meantime, PRRs trigger inflammatory signalling, with activation of transcription factors like nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB). NFκB is the key transcriptional regulator of many pro-inflammatory cytokines, adhesion molecules, chemokines, growth factors and other mediators of inflammation, as tumour necrosis factor (TNF), interleukins 1 (IL-1β), 6 (IL-6), and 12 (IL-12), promotes cellular proliferation and protects against apoptosis providing a mechanism that determines chronic inflammation. The recognition of pathogens is achieved through the presence of pattern recognition receptors (PRRs) [12]. PRRs identify the microbe-associated molecular patterns (MAMPs), and defensive responses is activated. PRRs include Toll-like receptors (TLRs), that are able to recognize viral DNA, viral double-stranded RNA and viral single-stranded RNA. TLRs are expressed on macrophages, dendritic cells, neutrophils, eosinophils, epithelial cells and keratinocytes. In particular, intracellular TLR-7 and TLR-8 allow the innate recognition of the single-stranded RNA of coronaviruses [13]. Intracellular and extracellular PRRs recognized spike glycoprotein, of the coronavirus coat, starting the inflammatory process, through the NFκB pathway [14]. Moreover, Nucleotide-Binding Domain, Leucine-Rich Repeat (NLR) proteins have also been identified, and NALP3 (NACHT, LRR and PYD domains-containing protein 3) has a special function in the innate immune response [15]. The processes involved in antiviral immunity is shown in Fig. 1.\nFig. 1 Graphical representation of antiviral SARS-Coronavirus 2 immunity. B: B lymphocyte; CTL: cytotoxic; T lymphocyte; IFN: interferon; Ig: immunoglobulin; IL: interleukin; MHC: major histocompatibility class; NFκB: nuclear factor kappa-light- chain- enhancer of activated B cells; NK: natural killer cell; Th: helper T lymphocyte; TLR: Toll-like receptor; TNF: tumour necrosis factor"}

LitCovid-PD-GO-BP

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T47","span":{"begin":0,"end":236},"obj":"Sentence"},{"id":"T48","span":{"begin":237,"end":326},"obj":"Sentence"},{"id":"T49","span":{"begin":327,"end":822},"obj":"Sentence"},{"id":"T50","span":{"begin":823,"end":916},"obj":"Sentence"},{"id":"T51","span":{"begin":917,"end":1088},"obj":"Sentence"},{"id":"T52","span":{"begin":1089,"end":1456},"obj":"Sentence"},{"id":"T53","span":{"begin":1457,"end":1564},"obj":"Sentence"},{"id":"T54","span":{"begin":1565,"end":1667},"obj":"Sentence"},{"id":"T55","span":{"begin":1668,"end":1803},"obj":"Sentence"},{"id":"T56","span":{"begin":1804,"end":1917},"obj":"Sentence"},{"id":"T57","span":{"begin":1918,"end":2041},"obj":"Sentence"},{"id":"T58","span":{"begin":2042,"end":2200},"obj":"Sentence"},{"id":"T59","span":{"begin":2201,"end":2418},"obj":"Sentence"},{"id":"T60","span":{"begin":2419,"end":2483},"obj":"Sentence"},{"id":"T61","span":{"begin":2484,"end":2557},"obj":"Sentence"},{"id":"T62","span":{"begin":2558,"end":2560},"obj":"Sentence"},{"id":"T63","span":{"begin":2561,"end":2822},"obj":"Sentence"},{"id":"T64","span":{"begin":2823,"end":2870},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"The binding of the cytokine to its transmembrane cell surface receptor activates an intracellular signal transduction pathway, generally a Janus kinase (Jak), which, via a kinase cascade, phosphorylates its transcription protein (STAT). Phosphorylated STAT dimers and moves to the nucleus, initiating a new gene transcription. Mutation of STAT1 increases susceptibility to virus infections because it is involved in various signalling pathways, including IFN-α/β, IFN- γ, IFN-l, IL-2, IL-3, IL-6, IL-9, IL-10, IL-11, IL-12, IL-15, IL-21, IL-22, IL-26 and IL-27 [10], and chemokines of several types such as C-X-C motif chemokine ligand 10 (CXCL-10), Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES)/Chemokine (C–C motif) ligand 5 (CCL-5), Monocyte Chemoattractant Protein-1 (MCP-1) [11]. IFN-γ promotes antigen-specific antibody production, increasing the activity of phagocytosis. In the meantime, PRRs trigger inflammatory signalling, with activation of transcription factors like nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB). NFκB is the key transcriptional regulator of many pro-inflammatory cytokines, adhesion molecules, chemokines, growth factors and other mediators of inflammation, as tumour necrosis factor (TNF), interleukins 1 (IL-1β), 6 (IL-6), and 12 (IL-12), promotes cellular proliferation and protects against apoptosis providing a mechanism that determines chronic inflammation. The recognition of pathogens is achieved through the presence of pattern recognition receptors (PRRs) [12]. PRRs identify the microbe-associated molecular patterns (MAMPs), and defensive responses is activated. PRRs include Toll-like receptors (TLRs), that are able to recognize viral DNA, viral double-stranded RNA and viral single-stranded RNA. TLRs are expressed on macrophages, dendritic cells, neutrophils, eosinophils, epithelial cells and keratinocytes. In particular, intracellular TLR-7 and TLR-8 allow the innate recognition of the single-stranded RNA of coronaviruses [13]. Intracellular and extracellular PRRs recognized spike glycoprotein, of the coronavirus coat, starting the inflammatory process, through the NFκB pathway [14]. Moreover, Nucleotide-Binding Domain, Leucine-Rich Repeat (NLR) proteins have also been identified, and NALP3 (NACHT, LRR and PYD domains-containing protein 3) has a special function in the innate immune response [15]. The processes involved in antiviral immunity is shown in Fig. 1.\nFig. 1 Graphical representation of antiviral SARS-Coronavirus 2 immunity. B: B lymphocyte; CTL: cytotoxic; T lymphocyte; IFN: interferon; Ig: immunoglobulin; IL: interleukin; MHC: major histocompatibility class; NFκB: nuclear factor kappa-light- chain- enhancer of activated B cells; NK: natural killer cell; Th: helper T lymphocyte; TLR: Toll-like receptor; TNF: tumour necrosis factor"}

LitCovid-PubTator

PMC:7647877 / 7001-9871 JSONTXT

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PMC:7647877 / 7001-9871 JSON TXT