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LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T50","span":{"begin":1548,"end":1553},"obj":"Body_part"}],"attributes":[{"id":"A50","pred":"uberon_id","subj":"T50","obj":"http://purl.obolibrary.org/obo/UBERON_0000062"}],"text":"A prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89"}

LitCovid-PD-MONDO

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T280","span":{"begin":0,"end":1},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T281","span":{"begin":270,"end":276},"obj":"http://purl.obolibrary.org/obo/CL_0000236"},{"id":"T282","span":{"begin":731,"end":732},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T283","span":{"begin":813,"end":819},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T284","span":{"begin":953,"end":959},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T285","span":{"begin":1117,"end":1125},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T286","span":{"begin":1126,"end":1133},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T287","span":{"begin":1233,"end":1242},"obj":"http://purl.obolibrary.org/obo/CHEBI_28790"},{"id":"T288","span":{"begin":1277,"end":1289},"obj":"http://purl.obolibrary.org/obo/CL_0000898"},{"id":"T289","span":{"begin":1290,"end":1300},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T290","span":{"begin":1377,"end":1383},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T291","span":{"begin":1469,"end":1470},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T292","span":{"begin":1521,"end":1528},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T293","span":{"begin":1534,"end":1539},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T294","span":{"begin":1548,"end":1553},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T295","span":{"begin":1565,"end":1566},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T296","span":{"begin":1698,"end":1708},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T297","span":{"begin":1712,"end":1719},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T298","span":{"begin":1808,"end":1815},"obj":"http://purl.obolibrary.org/obo/CL_0000084"}],"text":"A prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89"}

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T141","span":{"begin":1078,"end":1087},"obj":"Chemical"},{"id":"T142","span":{"begin":1224,"end":1226},"obj":"Chemical"},{"id":"T144","span":{"begin":1233,"end":1242},"obj":"Chemical"}],"attributes":[{"id":"A141","pred":"chebi_id","subj":"T141","obj":"http://purl.obolibrary.org/obo/CHEBI_25367"},{"id":"A142","pred":"chebi_id","subj":"T142","obj":"http://purl.obolibrary.org/obo/CHEBI_74795"},{"id":"A143","pred":"chebi_id","subj":"T142","obj":"http://purl.obolibrary.org/obo/CHEBI_90284"},{"id":"A144","pred":"chebi_id","subj":"T144","obj":"http://purl.obolibrary.org/obo/CHEBI_28790"},{"id":"A145","pred":"chebi_id","subj":"T144","obj":"http://purl.obolibrary.org/obo/CHEBI_350546"}],"text":"A prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89"}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T47","span":{"begin":1589,"end":1604},"obj":"Phenotype"},{"id":"T48","span":{"begin":1838,"end":1855},"obj":"Phenotype"}],"attributes":[{"id":"A47","pred":"hp_id","subj":"T47","obj":"http://purl.obolibrary.org/obo/HP_0006562"},{"id":"A48","pred":"hp_id","subj":"T48","obj":"http://purl.obolibrary.org/obo/HP_0004936"}],"text":"A prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89"}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T73","span":{"begin":218,"end":242},"obj":"http://purl.obolibrary.org/obo/GO_0002250"},{"id":"T74","span":{"begin":227,"end":242},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T75","span":{"begin":514,"end":538},"obj":"http://purl.obolibrary.org/obo/GO_0002250"},{"id":"T76","span":{"begin":523,"end":538},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T77","span":{"begin":1037,"end":1069},"obj":"http://purl.obolibrary.org/obo/GO_0046776"},{"id":"T78","span":{"begin":1140,"end":1172},"obj":"http://purl.obolibrary.org/obo/GO_0046776"},{"id":"T79","span":{"begin":1283,"end":1300},"obj":"http://purl.obolibrary.org/obo/GO_0042110"},{"id":"T80","span":{"begin":1285,"end":1300},"obj":"http://purl.obolibrary.org/obo/GO_0001775"},{"id":"T81","span":{"begin":1730,"end":1750},"obj":"http://purl.obolibrary.org/obo/GO_0070527"},{"id":"T82","span":{"begin":1877,"end":1898},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"A prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89"}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T104","span":{"begin":0,"end":580},"obj":"Sentence"},{"id":"T105","span":{"begin":581,"end":765},"obj":"Sentence"},{"id":"T106","span":{"begin":766,"end":1005},"obj":"Sentence"},{"id":"T107","span":{"begin":1006,"end":1335},"obj":"Sentence"},{"id":"T108","span":{"begin":1336,"end":1939},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"A prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89"}

2_test

{"project":"2_test","denotations":[{"id":"32586214-32346093-21597743","span":{"begin":344,"end":346},"obj":"32346093"},{"id":"32586214-20838746-21597744","span":{"begin":922,"end":924},"obj":"20838746"},{"id":"32586214-22706078-21597745","span":{"begin":1198,"end":1200},"obj":"22706078"},{"id":"32586214-24463452-21597746","span":{"begin":1270,"end":1272},"obj":"24463452"},{"id":"32586214-17158224-21597747","span":{"begin":1319,"end":1321},"obj":"17158224"},{"id":"32586214-16258538-21597748","span":{"begin":1605,"end":1607},"obj":"16258538"},{"id":"32586214-16634758-21597749","span":{"begin":1934,"end":1936},"obj":"16634758"},{"id":"32586214-27707800-21597750","span":{"begin":1937,"end":1939},"obj":"27707800"}],"text":"A prominent clinical feature of severe COVID-19 is the occurrence of respiratory decompensation typically 1 week after initial symptom onset.82 This clinical trajectory appears to correlate with the time course of the adaptive immune response to SARS-CoV-2, with T- and B-cell responses to SARS-CoV-2 being detected ≈1 week after symptom onset.46 Given it is postulated that this respiratory decompensation is driven by pulmonary microvascular thrombosis, understanding the intersection between thrombosis and the adaptive immune response to SARS-CoV-2 is of significant interest. These interactions are likely important since platelets have previously been demonstrated to be key modulators of adaptive immunity in the context of a range of inflammatory disorders. Platelets play an important role in regulating T-cell trafficking by facilitating the recruitment of T lymphocytes to sites of vascular injury or infection.83 Moreover, platelets enhance T-cell functional responses via multiple mechanisms. For example, platelets express major histocompatibility complex class 1 molecules and can, therefore, directly activate T cells in an major histocompatibility complex class 1 dependent manner,84 while platelet-derived PF-4 and serotonin can regulate Th17 expansion85 and naïve T-cell activation and proliferation,86 respectively. The importance of platelets in mediating T-cell recruitment and trafficking is underscored by data demonstrating that platelets play a fundamental role in the accumulation of cytotoxic T cells, and virus-induced organ damage, in a murine model of acute viral hepatitis.87 Akin to the bidirectional relationship between platelets and other leukocyte subsets, the activation of T cells amplifies platelet aggregation with more recent data highlighting an important role for T cells recruited to sites of venous thrombosis in orchestrating the inflammatory response and subsequent thrombus resolution.88,89"}

LitCovid-PubTator

PMC:7386875 / 28862-30801 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7386875 / 28862-30801 JSON TXT