PMC:1064895 / 2922-3699 JSONTXT

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{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T3484","span":{"begin":277,"end":281},"obj":"Protein"},{"id":"T3490","span":{"begin":403,"end":408},"obj":"Protein"},{"id":"T3489","span":{"begin":393,"end":398},"obj":"Protein"},{"id":"T3488","span":{"begin":386,"end":391},"obj":"Protein"},{"id":"T3487","span":{"begin":380,"end":384},"obj":"Protein"},{"id":"T3486","span":{"begin":374,"end":378},"obj":"Protein"},{"id":"T3485","span":{"begin":286,"end":298},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T3696","span":{"begin":386,"end":391},"obj":"http://www.uniprot.org/uniprot/P40933"},{"id":"T3693","span":{"begin":380,"end":384},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T3692","span":{"begin":286,"end":298},"obj":"http://www.uniprot.org/uniprot/P01579"},{"id":"T3691","span":{"begin":277,"end":281},"obj":"http://www.uniprot.org/uniprot/P60568"},{"id":"T3689","span":{"begin":403,"end":408},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T3687","span":{"begin":403,"end":406},"obj":"http://www.uniprot.org/uniprot/P01375"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"GO-BP","denotations":[{"id":"T2772","span":{"begin":502,"end":514},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T2771","span":{"begin":58,"end":70},"obj":"http://purl.obolibrary.org/obo/GO_0009405"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"GO-MF","denotations":[{"id":"T3525","span":{"begin":393,"end":398},"obj":"http://purl.obolibrary.org/obo/GO_0045515"},{"id":"T3523","span":{"begin":386,"end":391},"obj":"http://purl.obolibrary.org/obo/GO_0016170"},{"id":"T3520","span":{"begin":380,"end":384},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T3519","span":{"begin":286,"end":298},"obj":"http://purl.obolibrary.org/obo/GO_0005133"},{"id":"T3518","span":{"begin":277,"end":281},"obj":"http://purl.obolibrary.org/obo/GO_0005134"},{"id":"T3516","span":{"begin":374,"end":378},"obj":"http://purl.obolibrary.org/obo/GO_0005149"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"GO-CC","denotations":[{"id":"T3557","span":{"begin":727,"end":732},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3556","span":{"begin":612,"end":617},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3555","span":{"begin":489,"end":494},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3554","span":{"begin":45,"end":50},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"sentences","denotations":[{"id":"T2751","span":{"begin":0,"end":190},"obj":"Sentence"},{"id":"T2754","span":{"begin":526,"end":777},"obj":"Sentence"},{"id":"T2753","span":{"begin":447,"end":525},"obj":"Sentence"},{"id":"T2752","span":{"begin":191,"end":446},"obj":"Sentence"},{"id":"T21","span":{"begin":0,"end":190},"obj":"Sentence"},{"id":"T22","span":{"begin":191,"end":446},"obj":"Sentence"},{"id":"T23","span":{"begin":447,"end":525},"obj":"Sentence"},{"id":"T24","span":{"begin":526,"end":777},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"simple1","denotations":[{"id":"T3661","span":{"begin":403,"end":408},"obj":"Protein"},{"id":"T3660","span":{"begin":393,"end":398},"obj":"Protein"},{"id":"T3659","span":{"begin":386,"end":391},"obj":"Protein"},{"id":"T3658","span":{"begin":380,"end":384},"obj":"Protein"},{"id":"T3657","span":{"begin":374,"end":378},"obj":"Protein"},{"id":"T3656","span":{"begin":286,"end":298},"obj":"Protein"},{"id":"T3655","span":{"begin":277,"end":281},"obj":"Protein"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

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little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T3619","span":{"begin":633,"end":649},"obj":"Protein"},{"id":"T3618","span":{"begin":414,"end":422},"obj":"Gene_expression"},{"id":"T3617","span":{"begin":414,"end":422},"obj":"Gene_expression"},{"id":"T3616","span":{"begin":414,"end":422},"obj":"Gene_expression"},{"id":"T3615","span":{"begin":414,"end":422},"obj":"Gene_expression"},{"id":"T3614","span":{"begin":414,"end":422},"obj":"Gene_expression"},{"id":"T3613","span":{"begin":414,"end":422},"obj":"Gene_expression"},{"id":"T3612","span":{"begin":426,"end":445},"obj":"Protein"},{"id":"T3611","span":{"begin":403,"end":408},"obj":"Protein"},{"id":"T3610","span":{"begin":393,"end":398},"obj":"Protein"},{"id":"T3609","span":{"begin":386,"end":391},"obj":"Protein"},{"id":"T3608","span":{"begin":380,"end":384},"obj":"Protein"},{"id":"T3607","span":{"begin":374,"end":378},"obj":"Protein"},{"id":"T3606","span":{"begin":286,"end":298},"obj":"Protein"},{"id":"T3605","span":{"begin":277,"end":281},"obj":"Protein"}],"relations":[{"id":"R1754","pred":"themeOf","subj":"T3607","obj":"T3613"},{"id":"R1757","pred":"themeOf","subj":"T3608","obj":"T3614"},{"id":"R1758","pred":"themeOf","subj":"T3609","obj":"T3615"},{"id":"R1759","pred":"themeOf","subj":"T3610","obj":"T3616"},{"id":"R1760","pred":"themeOf","subj":"T3611","obj":"T3617"},{"id":"R1761","pred":"themeOf","subj":"T3612","obj":"T3618"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}

{"project":"testone","denotations":[{"id":"T2115","span":{"begin":403,"end":408},"obj":"Protein"},{"id":"T2114","span":{"begin":393,"end":398},"obj":"Protein"},{"id":"T2113","span":{"begin":386,"end":391},"obj":"Protein"},{"id":"T2112","span":{"begin":380,"end":384},"obj":"Protein"},{"id":"T2111","span":{"begin":374,"end":378},"obj":"Protein"},{"id":"T2110","span":{"begin":286,"end":298},"obj":"Protein"},{"id":"T2109","span":{"begin":277,"end":281},"obj":"Protein"}],"text":"A little over a decade ago, the primacy of T cells in the pathogenesis of autoimmune disease such as RA was undisputed because they are the largest cell population infiltrating the synovium. However, a series of studies demonstrated paucity of T cell-derived cytokines such as IL-2 and interferon-γ in the joints of RA, whereas macrophage and fibroblast cytokines including IL-1, IL-6, IL-15, IL-18 and TNF-α were abundant in rheumatoid synovium. This paradox has questioned the role of T cells in the pathogenesis of RA [3]. Because we have already demonstrated the enhanced proliferation of antigen specific T cells, especially to type II collagen, and the skewing of T helper type 1 (Th1) cytokines in RA [4], the role of T cells needs to be elucidated in different aspects."}