CORD-19:16a812de72963ceda960a168236e8dbe91832d45 / 20886-22549 JSONTXT

{"project":"CORD-19-SciBite-sentences","denotations":[{"id":"T226","span":{"begin":0,"end":1663},"obj":"http://www.genenames.org/cgi-bin/gene_symbol_report?match=CD4"},{"id":"T227","span":{"begin":0,"end":1663},"obj":"http://www.genenames.org/cgi-bin/gene_symbol_report?match=B2M"},{"id":"T228","span":{"begin":0,"end":1663},"obj":"http://purl.obolibrary.org/obo/HP0003447"},{"id":"T229","span":{"begin":0,"end":1663},"obj":"http://purl.obolibrary.org/obo/HP0000707"},{"id":"T231","span":{"begin":0,"end":1663},"obj":"http://purl.obolibrary.org/obo/HP0011096"},{"id":"T232","span":{"begin":0,"end":1663},"obj":"https://id.nlm.nih.gov/mesh/D006801"},{"id":"T238","span":{"begin":0,"end":1663},"obj":"https://id.nlm.nih.gov/mesh/D051379"},{"id":"T239","span":{"begin":0,"end":1663},"obj":"http://purl.obolibrary.org/obo/GO0030424"},{"id":"T245","span":{"begin":0,"end":1663},"obj":"https://id.nlm.nih.gov/mesh/D003711"},{"id":"T247","span":{"begin":0,"end":1663},"obj":"https://id.nlm.nih.gov/mesh/D009461"}],"attributes":[{"id":"A226","pred":"class","subj":"T226","obj":"GENE"},{"id":"A227","pred":"class","subj":"T227","obj":"GENE"},{"id":"A228","pred":"class","subj":"T228","obj":"HPO"},{"id":"A229","pred":"class","subj":"T229","obj":"HPO"},{"id":"A231","pred":"class","subj":"T231","obj":"HPO"},{"id":"A232","pred":"class","subj":"T232","obj":"SPECIES"},{"id":"A238","pred":"class","subj":"T238","obj":"SPECIES"},{"id":"A239","pred":"class","subj":"T239","obj":"GOONTOL"},{"id":"A245","pred":"class","subj":"T245","obj":"INDICATION"},{"id":"A247","pred":"class","subj":"T247","obj":"INDICATION"}],"text":"For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS."}

{"project":"CORD-19_Custom_license_subset","denotations":[{"id":"T106","span":{"begin":0,"end":451},"obj":"Sentence"},{"id":"T107","span":{"begin":452,"end":709},"obj":"Sentence"},{"id":"T108","span":{"begin":710,"end":896},"obj":"Sentence"},{"id":"T109","span":{"begin":897,"end":1235},"obj":"Sentence"},{"id":"T110","span":{"begin":1236,"end":1542},"obj":"Sentence"},{"id":"T111","span":{"begin":1543,"end":1663},"obj":"Sentence"}],"text":"For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS."}

{"project":"CORD-19-Sentences","denotations":[{"id":"TextSentencer_T106","span":{"begin":0,"end":451},"obj":"Sentence"},{"id":"TextSentencer_T107","span":{"begin":452,"end":709},"obj":"Sentence"},{"id":"TextSentencer_T108","span":{"begin":710,"end":896},"obj":"Sentence"},{"id":"TextSentencer_T109","span":{"begin":897,"end":1235},"obj":"Sentence"},{"id":"TextSentencer_T110","span":{"begin":1236,"end":1542},"obj":"Sentence"},{"id":"TextSentencer_T111","span":{"begin":1543,"end":1663},"obj":"Sentence"},{"id":"TextSentencer_T106","span":{"begin":0,"end":451},"obj":"Sentence"},{"id":"TextSentencer_T107","span":{"begin":452,"end":709},"obj":"Sentence"},{"id":"TextSentencer_T108","span":{"begin":710,"end":896},"obj":"Sentence"},{"id":"TextSentencer_T109","span":{"begin":897,"end":1235},"obj":"Sentence"},{"id":"TextSentencer_T110","span":{"begin":1236,"end":1542},"obj":"Sentence"},{"id":"TextSentencer_T111","span":{"begin":1543,"end":1663},"obj":"Sentence"},{"id":"T46970","span":{"begin":0,"end":451},"obj":"Sentence"},{"id":"T95181","span":{"begin":452,"end":709},"obj":"Sentence"},{"id":"T44800","span":{"begin":710,"end":896},"obj":"Sentence"},{"id":"T29420","span":{"begin":897,"end":1235},"obj":"Sentence"},{"id":"T42580","span":{"begin":1236,"end":1542},"obj":"Sentence"},{"id":"T78951","span":{"begin":1543,"end":1663},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS."}

{"project":"Epistemic_Statements","denotations":[{"id":"T49","span":{"begin":0,"end":451},"obj":"Epistemic_statement"},{"id":"T50","span":{"begin":452,"end":709},"obj":"Epistemic_statement"},{"id":"T51","span":{"begin":710,"end":896},"obj":"Epistemic_statement"},{"id":"T52","span":{"begin":897,"end":1235},"obj":"Epistemic_statement"},{"id":"T53","span":{"begin":1236,"end":1542},"obj":"Epistemic_statement"},{"id":"T54","span":{"begin":1543,"end":1663},"obj":"Epistemic_statement"}],"text":"For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS."}

{"project":"CORD-19-PD-MONDO","denotations":[{"id":"T76","span":{"begin":549,"end":551},"obj":"Disease"},{"id":"T77","span":{"begin":816,"end":818},"obj":"Disease"},{"id":"T78","span":{"begin":863,"end":865},"obj":"Disease"},{"id":"T79","span":{"begin":1063,"end":1065},"obj":"Disease"},{"id":"T80","span":{"begin":1199,"end":1205},"obj":"Disease"},{"id":"T81","span":{"begin":1209,"end":1211},"obj":"Disease"},{"id":"T82","span":{"begin":1426,"end":1428},"obj":"Disease"},{"id":"T83","span":{"begin":1624,"end":1630},"obj":"Disease"},{"id":"T84","span":{"begin":1660,"end":1662},"obj":"Disease"}],"attributes":[{"id":"A76","pred":"mondo_id","subj":"T76","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A77","pred":"mondo_id","subj":"T77","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A78","pred":"mondo_id","subj":"T78","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A79","pred":"mondo_id","subj":"T79","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A80","pred":"mondo_id","subj":"T80","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A81","pred":"mondo_id","subj":"T81","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A82","pred":"mondo_id","subj":"T82","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A83","pred":"mondo_id","subj":"T83","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A84","pred":"mondo_id","subj":"T84","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"}],"text":"For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS."}

{"project":"CORD-19-PD-HP","denotations":[{"id":"T53","span":{"begin":112,"end":125},"obj":"Phenotype"},{"id":"T54","span":{"begin":366,"end":379},"obj":"Phenotype"},{"id":"T55","span":{"begin":575,"end":588},"obj":"Phenotype"},{"id":"T56","span":{"begin":1411,"end":1422},"obj":"Phenotype"}],"attributes":[{"id":"A53","pred":"hp_id","subj":"T53","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A54","pred":"hp_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A55","pred":"hp_id","subj":"T55","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A56","pred":"hp_id","subj":"T56","obj":"http://purl.obolibrary.org/obo/HP_0003447"}],"text":"For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS."}

{"project":"CORD-19-PD-UBERON","denotations":[{"id":"T55","span":{"begin":326,"end":332},"obj":"Body_part"},{"id":"T56","span":{"begin":819,"end":824},"obj":"Body_part"}],"attributes":[{"id":"A55","pred":"uberon_id","subj":"T55","obj":"http://purl.obolibrary.org/obo/UBERON_0000345"},{"id":"A56","pred":"uberon_id","subj":"T56","obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS."}