CORD-19:68a7101a90454172c91785d8c352f776a82df5d4 / 360743-360963 JSONTXT

{"project":"CORD-19-Sentences","denotations":[{"id":"T65465","span":{"begin":0,"end":220},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"MS remission signature was characterized by a further suppression of Th1 response (TBX21 and CD58) associated with activation of negative regulators of NFkB dependent inflammation (TNFAIP3) and cytokine signaling (SOCS)."}

{"project":"CORD-19_Custom_license_subset","denotations":[{"id":"T83","span":{"begin":0,"end":220},"obj":"Sentence"}],"text":"MS remission signature was characterized by a further suppression of Th1 response (TBX21 and CD58) associated with activation of negative regulators of NFkB dependent inflammation (TNFAIP3) and cytokine signaling (SOCS)."}

{"project":"CORD-19-PD-UBERON","denotations":[{"id":"T1464","span":{"begin":0,"end":2},"obj":"Body_part"}],"attributes":[{"id":"A1464","pred":"uberon_id","subj":"T1464","obj":"http://purl.obolibrary.org/obo/UBERON_0001877"}],"text":"MS remission signature was characterized by a further suppression of Th1 response (TBX21 and CD58) associated with activation of negative regulators of NFkB dependent inflammation (TNFAIP3) and cytokine signaling (SOCS)."}

{"project":"CORD-19-PD-MONDO","denotations":[{"id":"T2342","span":{"begin":0,"end":2},"obj":"Disease"},{"id":"T2343","span":{"begin":167,"end":179},"obj":"Disease"},{"id":"T92243","span":{"begin":0,"end":2},"obj":"Disease"},{"id":"T47862","span":{"begin":167,"end":179},"obj":"Disease"}],"attributes":[{"id":"A2342","pred":"mondo_id","subj":"T2342","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A2343","pred":"mondo_id","subj":"T2343","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A63397","pred":"mondo_id","subj":"T92243","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A65615","pred":"mondo_id","subj":"T47862","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"}],"text":"MS remission signature was characterized by a further suppression of Th1 response (TBX21 and CD58) associated with activation of negative regulators of NFkB dependent inflammation (TNFAIP3) and cytokine signaling (SOCS)."}