PMC:1064895 / 2407-5647 JSON TXT

Annnotations TAB JSON ListView MergeView

test3

BioNLP16_Messiy

BioNLP16_DUT

2_test

{"project":"2_test","denotations":[{"id":"15642134-12810425-4202008","span":{"begin":256,"end":257},"obj":"12810425"},{"id":"15642134-12810200-4202009","span":{"begin":511,"end":512},"obj":"12810200"},{"id":"15642134-9683554-4202010","span":{"begin":1037,"end":1038},"obj":"9683554"},{"id":"15642134-10524679-4202011","span":{"begin":1224,"end":1225},"obj":"10524679"},{"id":"15642134-8676080-4202012","span":{"begin":1421,"end":1422},"obj":"8676080"},{"id":"15642134-12632409-4202013","span":{"begin":1586,"end":1587},"obj":"12632409"},{"id":"15642134-12594294-4202014","span":{"begin":1806,"end":1807},"obj":"12594294"},{"id":"15642134-9182915-4202015","span":{"begin":2029,"end":2030},"obj":"9182915"},{"id":"15642134-11669582-4202015","span":{"begin":2029,"end":2030},"obj":"11669582"},{"id":"15642134-11592370-4202015","span":{"begin":2029,"end":2030},"obj":"11592370"},{"id":"15642134-10225978-4202016","span":{"begin":2213,"end":2215},"obj":"10225978"},{"id":"15642134-10323452-4202017","span":{"begin":2216,"end":2218},"obj":"10323452"},{"id":"15642134-10679127-4202018","span":{"begin":2426,"end":2428},"obj":"10679127"},{"id":"15642134-12707317-4202019","span":{"begin":2569,"end":2571},"obj":"12707317"},{"id":"15642134-10323452-4202020","span":{"begin":2677,"end":2679},"obj":"10323452"},{"id":"15642134-12677240-4202021","span":{"begin":2680,"end":2682},"obj":"12677240"},{"id":"15642134-15022319-4202022","span":{"begin":2683,"end":2685},"obj":"15022319"}],"text":"Introduction\nRheumatoid arthritis (RA) is characterized by infiltrations of macrophages and T cells into the joint, and synovial hyperplasia. Proinflammatory cytokines released from these cells are known to be important in the destruction of joints in RA [1]. The favorable clinical benefits obtained with inhibitors of tumor necrosis factor (TNF)-α) and interleukin (IL)-1 suggest that the blockade of key inflammatory cytokines has been the important issue in the development of new therapeutic applications [2].\nA 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.\nIL-17 is one of the inflammatory cytokines secreted mainly by activated T cells, which can induce IL-6 and IL-8 by fibroblasts [5]. This cytokine is of interest for two major reasons: first, similarly to TNF-α and IL-1, IL-17 has proinflammatory properties; second, it is produced by T cells [6]. Recent observations demonstrated that IL-17 can also activate osteoclastic bone resorption by the induction of RANKL (receptor activator of nuclear factor κB [NF-κB] ligand), which is involved in bony erosion in RA [7]. It also stimulates the production of IL-6 and leukemia inhibitory factor by synoviocytes, and of prostaglandin E2 and nitric oxide by chondrocytes, and has the ability to differentiate and activate the dendritic cells [8-10]. Levels of IL-17 in synovial fluids were significantly higher in patients with RA than in patients with osteoarthritis (OA), and it was produced by CD4+ T cells in the synovium [11,12].\nIL-15, secreted from activated macrophages, has been reported to be an important trigger of IL-17 production in RA peripheral blood mononuclear cells (PBMC) by cyclosporine and steroid sensitive pathways [13]. Recently, Happel and colleagues also showed that IL-23 could be an efficient trigger of IL-17 production from both CD4+ and CD8+ T cells [14].\nAlthough the contribution of IL-17 in joint inflammation in RA has been documented in earlier studies [12,15,16], the intracellular signal transduction pathway for IL-17 production remains uncertain. In the present study we used various stimuli to investigate IL-17 production in PBMC of patients with RA and its signaling transduction pathway.\nWe found that the intracellular signaling pathway involving phosphoinositide 3-kinase (PI3K)/Akt and NF-κB might be involved in the overproduction of the key inflammatory cytokine IL-17 in RA. These results might provide new insights into the pathogenesis of RA and future directions for new therapeutic strategies in RA."}

biosemtest

pmc-enju-pas

bionlp-st-ge-2016-coref

bionlp-st-ge-2016-test-proteins

bionlp-st-ge-2016-uniprot

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T2234","span":{"begin":2347,"end":2352},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T2233","span":{"begin":2055,"end":2070},"obj":"http://purl.obolibrary.org/obo/UBERON_0001090"}],"text":"Introduction\nRheumatoid arthritis (RA) is characterized by infiltrations of macrophages and T cells into the joint, and synovial hyperplasia. Proinflammatory cytokines released from these cells are known to be important in the destruction of joints in RA [1]. The favorable clinical benefits obtained with inhibitors of tumor necrosis factor (TNF)-α) and interleukin (IL)-1 suggest that the blockade of key inflammatory cytokines has been the important issue in the development of new therapeutic applications [2].\nA 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.\nIL-17 is one of the inflammatory cytokines secreted mainly by activated T cells, which can induce IL-6 and IL-8 by fibroblasts [5]. This cytokine is of interest for two major reasons: first, similarly to TNF-α and IL-1, IL-17 has proinflammatory properties; second, it is produced by T cells [6]. Recent observations demonstrated that IL-17 can also activate osteoclastic bone resorption by the induction of RANKL (receptor activator of nuclear factor κB [NF-κB] ligand), which is involved in bony erosion in RA [7]. It also stimulates the production of IL-6 and leukemia inhibitory factor by synoviocytes, and of prostaglandin E2 and nitric oxide by chondrocytes, and has the ability to differentiate and activate the dendritic cells [8-10]. Levels of IL-17 in synovial fluids were significantly higher in patients with RA than in patients with osteoarthritis (OA), and it was produced by CD4+ T cells in the synovium [11,12].\nIL-15, secreted from activated macrophages, has been reported to be an important trigger of IL-17 production in RA peripheral blood mononuclear cells (PBMC) by cyclosporine and steroid sensitive pathways [13]. Recently, Happel and colleagues also showed that IL-23 could be an efficient trigger of IL-17 production from both CD4+ and CD8+ T cells [14].\nAlthough the contribution of IL-17 in joint inflammation in RA has been documented in earlier studies [12,15,16], the intracellular signal transduction pathway for IL-17 production remains uncertain. In the present study we used various stimuli to investigate IL-17 production in PBMC of patients with RA and its signaling transduction pathway.\nWe found that the intracellular signaling pathway involving phosphoinositide 3-kinase (PI3K)/Akt and NF-κB might be involved in the overproduction of the key inflammatory cytokine IL-17 in RA. These results might provide new insights into the pathogenesis of RA and future directions for new therapeutic strategies in RA."}

GO-BP

GO-MF

GO-CC

{"project":"GO-CC","denotations":[{"id":"T3565","span":{"begin":2937,"end":2950},"obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"T3564","span":{"begin":2692,"end":2705},"obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"T3563","span":{"begin":2562,"end":2567},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3562","span":{"begin":2365,"end":2370},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3561","span":{"begin":2190,"end":2195},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3560","span":{"begin":2022,"end":2027},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3559","span":{"begin":1579,"end":1584},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3558","span":{"begin":1367,"end":1372},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3557","span":{"begin":1242,"end":1247},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3556","span":{"begin":1127,"end":1132},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3555","span":{"begin":1004,"end":1009},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3554","span":{"begin":560,"end":565},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3553","span":{"begin":188,"end":193},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3552","span":{"begin":94,"end":99},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Introduction\nRheumatoid arthritis (RA) is characterized by infiltrations of macrophages and T cells into the joint, and synovial hyperplasia. Proinflammatory cytokines released from these cells are known to be important in the destruction of joints in RA [1]. The favorable clinical benefits obtained with inhibitors of tumor necrosis factor (TNF)-α) and interleukin (IL)-1 suggest that the blockade of key inflammatory cytokines has been the important issue in the development of new therapeutic applications [2].\nA 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.\nIL-17 is one of the inflammatory cytokines secreted mainly by activated T cells, which can induce IL-6 and IL-8 by fibroblasts [5]. This cytokine is of interest for two major reasons: first, similarly to TNF-α and IL-1, IL-17 has proinflammatory properties; second, it is produced by T cells [6]. Recent observations demonstrated that IL-17 can also activate osteoclastic bone resorption by the induction of RANKL (receptor activator of nuclear factor κB [NF-κB] ligand), which is involved in bony erosion in RA [7]. It also stimulates the production of IL-6 and leukemia inhibitory factor by synoviocytes, and of prostaglandin E2 and nitric oxide by chondrocytes, and has the ability to differentiate and activate the dendritic cells [8-10]. Levels of IL-17 in synovial fluids were significantly higher in patients with RA than in patients with osteoarthritis (OA), and it was produced by CD4+ T cells in the synovium [11,12].\nIL-15, secreted from activated macrophages, has been reported to be an important trigger of IL-17 production in RA peripheral blood mononuclear cells (PBMC) by cyclosporine and steroid sensitive pathways [13]. Recently, Happel and colleagues also showed that IL-23 could be an efficient trigger of IL-17 production from both CD4+ and CD8+ T cells [14].\nAlthough the contribution of IL-17 in joint inflammation in RA has been documented in earlier studies [12,15,16], the intracellular signal transduction pathway for IL-17 production remains uncertain. In the present study we used various stimuli to investigate IL-17 production in PBMC of patients with RA and its signaling transduction pathway.\nWe found that the intracellular signaling pathway involving phosphoinositide 3-kinase (PI3K)/Akt and NF-κB might be involved in the overproduction of the key inflammatory cytokine IL-17 in RA. These results might provide new insights into the pathogenesis of RA and future directions for new therapeutic strategies in RA."}

sentences

ICD10

{"project":"ICD10","denotations":[{"id":"T3567","span":{"begin":24,"end":33},"obj":"http://purl.bioontology.org/ontology/ICD10/M13.9"},{"id":"T3566","span":{"begin":13,"end":33},"obj":"http://purl.bioontology.org/ontology/ICD10/M06.9"}],"text":"Introduction\nRheumatoid arthritis (RA) is characterized by infiltrations of macrophages and T cells into the joint, and synovial hyperplasia. Proinflammatory cytokines released from these cells are known to be important in the destruction of joints in RA [1]. The favorable clinical benefits obtained with inhibitors of tumor necrosis factor (TNF)-α) and interleukin (IL)-1 suggest that the blockade of key inflammatory cytokines has been the important issue in the development of new therapeutic applications [2].\nA 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.\nIL-17 is one of the inflammatory cytokines secreted mainly by activated T cells, which can induce IL-6 and IL-8 by fibroblasts [5]. This cytokine is of interest for two major reasons: first, similarly to TNF-α and IL-1, IL-17 has proinflammatory properties; second, it is produced by T cells [6]. Recent observations demonstrated that IL-17 can also activate osteoclastic bone resorption by the induction of RANKL (receptor activator of nuclear factor κB [NF-κB] ligand), which is involved in bony erosion in RA [7]. It also stimulates the production of IL-6 and leukemia inhibitory factor by synoviocytes, and of prostaglandin E2 and nitric oxide by chondrocytes, and has the ability to differentiate and activate the dendritic cells [8-10]. Levels of IL-17 in synovial fluids were significantly higher in patients with RA than in patients with osteoarthritis (OA), and it was produced by CD4+ T cells in the synovium [11,12].\nIL-15, secreted from activated macrophages, has been reported to be an important trigger of IL-17 production in RA peripheral blood mononuclear cells (PBMC) by cyclosporine and steroid sensitive pathways [13]. Recently, Happel and colleagues also showed that IL-23 could be an efficient trigger of IL-17 production from both CD4+ and CD8+ T cells [14].\nAlthough the contribution of IL-17 in joint inflammation in RA has been documented in earlier studies [12,15,16], the intracellular signal transduction pathway for IL-17 production remains uncertain. In the present study we used various stimuli to investigate IL-17 production in PBMC of patients with RA and its signaling transduction pathway.\nWe found that the intracellular signaling pathway involving phosphoinositide 3-kinase (PI3K)/Akt and NF-κB might be involved in the overproduction of the key inflammatory cytokine IL-17 in RA. These results might provide new insights into the pathogenesis of RA and future directions for new therapeutic strategies in RA."}

simple1

DLUT931

bionlp-st-ge-2016-test-ihmc

bionlp-st-ge-2016-spacy-parsed

bionlp-st-ge-2016-test-tees

testone

PMC:1064895 / 2407-5647 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:1064895 / 2407-5647 JSON TXT