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Glycan-Motif

GlyCosmos6-Glycan-Motif-Image

Glycosmos6-GlycoEpitope

{"project":"Glycosmos6-GlycoEpitope","denotations":[{"id":"T1","span":{"begin":256,"end":259},"obj":"http://www.glycoepitope.jp/epitopes/EP0050"},{"id":"T2","span":{"begin":261,"end":265},"obj":"http://www.glycoepitope.jp/epitopes/EP0056"},{"id":"T3","span":{"begin":267,"end":271},"obj":"http://www.glycoepitope.jp/epitopes/EP0059"},{"id":"T4","span":{"begin":273,"end":277},"obj":"http://www.glycoepitope.jp/epitopes/EP0067"},{"id":"T5","span":{"begin":283,"end":287},"obj":"http://www.glycoepitope.jp/epitopes/EP0069"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

Glycosmos6-MAT

{"project":"Glycosmos6-MAT","denotations":[{"id":"T1","span":{"begin":1177,"end":1181},"obj":"http://purl.obolibrary.org/obo/MAT_0000091"},{"id":"T2","span":{"begin":1237,"end":1259},"obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"T3","span":{"begin":1245,"end":1259},"obj":"http://purl.obolibrary.org/obo/MAT_0000026"},{"id":"T4","span":{"begin":1261,"end":1264},"obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"T5","span":{"begin":1342,"end":1345},"obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"T6","span":{"begin":1561,"end":1564},"obj":"http://purl.obolibrary.org/obo/MAT_0000457"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

sentences

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":94},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":95,"end":374},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":375,"end":441},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":442,"end":619},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":620,"end":778},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":779,"end":937},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":938,"end":1163},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":1164,"end":1429},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":1430,"end":1565},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":1566,"end":1691},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":94},"obj":"Sentence"},{"id":"T2","span":{"begin":95,"end":374},"obj":"Sentence"},{"id":"T3","span":{"begin":375,"end":441},"obj":"Sentence"},{"id":"T4","span":{"begin":442,"end":619},"obj":"Sentence"},{"id":"T5","span":{"begin":620,"end":778},"obj":"Sentence"},{"id":"T6","span":{"begin":779,"end":937},"obj":"Sentence"},{"id":"T7","span":{"begin":938,"end":1163},"obj":"Sentence"},{"id":"T8","span":{"begin":1164,"end":1429},"obj":"Sentence"},{"id":"T9","span":{"begin":1430,"end":1565},"obj":"Sentence"},{"id":"T10","span":{"begin":1566,"end":1691},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":94},"obj":"Sentence"},{"id":"T2","span":{"begin":95,"end":374},"obj":"Sentence"},{"id":"T3","span":{"begin":375,"end":441},"obj":"Sentence"},{"id":"T4","span":{"begin":442,"end":619},"obj":"Sentence"},{"id":"T5","span":{"begin":620,"end":778},"obj":"Sentence"},{"id":"T6","span":{"begin":779,"end":937},"obj":"Sentence"},{"id":"T7","span":{"begin":938,"end":1163},"obj":"Sentence"},{"id":"T8","span":{"begin":1164,"end":1429},"obj":"Sentence"},{"id":"T9","span":{"begin":1430,"end":1565},"obj":"Sentence"},{"id":"T10","span":{"begin":1566,"end":1691},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos6-Glycan-Motif-Structure

ICD10

{"project":"ICD10","denotations":[{"id":"T1","span":{"begin":1237,"end":1259},"obj":"http://purl.bioontology.org/ontology/ICD10/B69.0"},{"id":"T2","span":{"begin":1237,"end":1259},"obj":"http://purl.bioontology.org/ontology/ICD10/G96.9"},{"id":"T3","span":{"begin":1245,"end":1252},"obj":"http://purl.bioontology.org/ontology/ICD10/R45.0"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

uniprot-human

{"project":"uniprot-human","denotations":[{"id":"T1","span":{"begin":157,"end":173},"obj":"http://www.uniprot.org/uniprot/Q00973"},{"id":"T2","span":{"begin":383,"end":418},"obj":"http://www.uniprot.org/uniprot/Q96KV0"},{"id":"T3","span":{"begin":420,"end":423},"obj":"http://www.uniprot.org/uniprot/Q96KV0"},{"id":"T4","span":{"begin":640,"end":643},"obj":"http://www.uniprot.org/uniprot/Q96KV0"},{"id":"T5","span":{"begin":812,"end":815},"obj":"http://www.uniprot.org/uniprot/Q96KV0"},{"id":"T6","span":{"begin":961,"end":964},"obj":"http://www.uniprot.org/uniprot/Q96KV0"},{"id":"T7","span":{"begin":383,"end":418},"obj":"http://www.uniprot.org/uniprot/P23515"},{"id":"T8","span":{"begin":1318,"end":1321},"obj":"http://www.uniprot.org/uniprot/P01730"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

uniprot-mouse

{"project":"uniprot-mouse","denotations":[{"id":"T1","span":{"begin":157,"end":173},"obj":"http://www.uniprot.org/uniprot/Q09200"},{"id":"T2","span":{"begin":383,"end":418},"obj":"http://www.uniprot.org/uniprot/Q61885"},{"id":"T3","span":{"begin":383,"end":418},"obj":"http://www.uniprot.org/uniprot/Q63912"},{"id":"T4","span":{"begin":1318,"end":1321},"obj":"http://www.uniprot.org/uniprot/P06332"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlycoBiology-NCBITAXON

{"project":"GlycoBiology-NCBITAXON","denotations":[{"id":"T1","span":{"begin":655,"end":660},"obj":"http://purl.bioontology.org/ontology/STY/T025"},{"id":"T2","span":{"begin":771,"end":777},"obj":"http://purl.bioontology.org/ontology/STY/T096"},{"id":"T3","span":{"begin":827,"end":832},"obj":"http://purl.bioontology.org/ontology/STY/T025"},{"id":"T4","span":{"begin":976,"end":981},"obj":"http://purl.bioontology.org/ontology/STY/T025"},{"id":"T5","span":{"begin":1018,"end":1023},"obj":"http://purl.bioontology.org/ontology/STY/T025"},{"id":"T6","span":{"begin":1269,"end":1272},"obj":"http://purl.bioontology.org/ontology/NCBITAXON/82391"},{"id":"T7","span":{"begin":1546,"end":1551},"obj":"http://purl.bioontology.org/ontology/STY/T025"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T1","span":{"begin":37,"end":48},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T2","span":{"begin":157,"end":173},"obj":"http://purl.obolibrary.org/obo/GO_0003947"},{"id":"T3","span":{"begin":345,"end":357},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T4","span":{"begin":383,"end":389},"obj":"http://purl.obolibrary.org/obo/GO_0042552"},{"id":"T5","span":{"begin":999,"end":1017},"obj":"http://purl.obolibrary.org/obo/GO_0019882"},{"id":"T6","span":{"begin":1208,"end":1216},"obj":"http://purl.obolibrary.org/obo/GO_0007349"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T1","span":{"begin":655,"end":660},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T2","span":{"begin":827,"end":832},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T3","span":{"begin":976,"end":981},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T4","span":{"begin":1018,"end":1023},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5","span":{"begin":1323,"end":1327},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6","span":{"begin":1622,"end":1626},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T7","span":{"begin":1639,"end":1643},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T1","span":{"begin":383,"end":389},"obj":"http://purl.obolibrary.org/obo/UBERON_0000345"},{"id":"T2","span":{"begin":1080,"end":1091},"obj":"http://purl.obolibrary.org/obo/UBERON_0001986"},{"id":"T3","span":{"begin":1237,"end":1244},"obj":"http://purl.obolibrary.org/obo/UBERON_0012131"},{"id":"T4","span":{"begin":1237,"end":1259},"obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"T5","span":{"begin":1245,"end":1259},"obj":"http://purl.obolibrary.org/obo/UBERON_0001016"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlycoBiology-MAT

{"project":"GlycoBiology-MAT","denotations":[{"id":"T1","span":{"begin":1177,"end":1181},"obj":"http://purl.obolibrary.org/obo/MAT_0000091"},{"id":"T2","span":{"begin":1237,"end":1259},"obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"T3","span":{"begin":1245,"end":1259},"obj":"http://purl.obolibrary.org/obo/MAT_0000026"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlycoBiology-Epitope

{"project":"GlycoBiology-Epitope","denotations":[{"id":"PD-GlycoEpitope-B_T1","span":{"begin":161,"end":164},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T2","span":{"begin":193,"end":196},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T3","span":{"begin":574,"end":577},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T4","span":{"begin":670,"end":673},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T5","span":{"begin":860,"end":863},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T6","span":{"begin":913,"end":916},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T7","span":{"begin":1137,"end":1140},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T8","span":{"begin":1364,"end":1367},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T9","span":{"begin":1480,"end":1483},"obj":"http://www.glycoepitope.jp/epitopes/EP0061"},{"id":"PD-GlycoEpitope-B_T10","span":{"begin":256,"end":259},"obj":"http://www.glycoepitope.jp/epitopes/EP0050"},{"id":"PD-GlycoEpitope-B_T11","span":{"begin":261,"end":265},"obj":"http://www.glycoepitope.jp/epitopes/EP0056"},{"id":"PD-GlycoEpitope-B_T12","span":{"begin":267,"end":271},"obj":"http://www.glycoepitope.jp/epitopes/EP0059"},{"id":"PD-GlycoEpitope-B_T13","span":{"begin":273,"end":277},"obj":"http://www.glycoepitope.jp/epitopes/EP0067"},{"id":"PD-GlycoEpitope-B_T14","span":{"begin":283,"end":287},"obj":"http://www.glycoepitope.jp/epitopes/EP0069"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

performance-test

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":1237,"end":1244},"obj":"http://purl.obolibrary.org/obo/UBERON_0012131"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1237,"end":1259},"obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1245,"end":1259},"obj":"http://purl.obolibrary.org/obo/UBERON_0001016"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":383,"end":389},"obj":"http://purl.obolibrary.org/obo/UBERON_0000345"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":1080,"end":1091},"obj":"http://purl.obolibrary.org/obo/UBERON_0001986"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

mondo_disease

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":52,"end":93},"obj":"Disease"},{"id":"T2","span":{"begin":106,"end":147},"obj":"Disease"},{"id":"T3","span":{"begin":149,"end":152},"obj":"Disease"},{"id":"T4","span":{"begin":465,"end":468},"obj":"Disease"},{"id":"T5","span":{"begin":902,"end":905},"obj":"Disease"},{"id":"T6","span":{"begin":1298,"end":1301},"obj":"Disease"},{"id":"T7","span":{"begin":1469,"end":1472},"obj":"Disease"},{"id":"T8","span":{"begin":1687,"end":1690},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/MONDO_0005134"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

Anatomy-MAT

{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":1177,"end":1181},"obj":"Body_part"},{"id":"T2","span":{"begin":1237,"end":1259},"obj":"Body_part"},{"id":"T3","span":{"begin":1261,"end":1264},"obj":"Body_part"},{"id":"T4","span":{"begin":1342,"end":1345},"obj":"Body_part"},{"id":"T5","span":{"begin":1561,"end":1564},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000091"},{"id":"A2","pred":"mat_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"A3","pred":"mat_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"A4","pred":"mat_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"A5","pred":"mat_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MAT_0000457"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

Glycan-GlyCosmos

GlyCosmos15-MONDO

{"project":"GlyCosmos15-MONDO","denotations":[{"id":"T1","span":{"begin":52,"end":93},"obj":"Disease"},{"id":"T2","span":{"begin":106,"end":147},"obj":"Disease"},{"id":"T3","span":{"begin":149,"end":152},"obj":"Disease"},{"id":"T4","span":{"begin":465,"end":468},"obj":"Disease"},{"id":"T5","span":{"begin":902,"end":905},"obj":"Disease"},{"id":"T6","span":{"begin":1298,"end":1301},"obj":"Disease"},{"id":"T7","span":{"begin":1469,"end":1472},"obj":"Disease"},{"id":"T8","span":{"begin":1687,"end":1690},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"MONDO:0005134"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"MONDO:0005134"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"MONDO:0005134"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"MONDO:0005134"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"MONDO:0005134"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"MONDO:0005134"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"MONDO:0005134"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"MONDO:0005134"}],"namespaces":[{"prefix":"MONDO","uri":"http://purl.obolibrary.org/obo/MONDO_"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos15-NCBITAXON

{"project":"GlyCosmos15-NCBITAXON","denotations":[{"id":"T1","span":{"begin":183,"end":187},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":614,"end":618},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":690,"end":694},"obj":"OrganismTaxon"},{"id":"T4","span":{"begin":708,"end":712},"obj":"OrganismTaxon"},{"id":"T5","span":{"begin":848,"end":852},"obj":"OrganismTaxon"},{"id":"T6","span":{"begin":883,"end":887},"obj":"OrganismTaxon"},{"id":"T7","span":{"begin":920,"end":924},"obj":"OrganismTaxon"},{"id":"T8","span":{"begin":1158,"end":1162},"obj":"OrganismTaxon"},{"id":"T9","span":{"begin":1371,"end":1375},"obj":"OrganismTaxon"},{"id":"T10","span":{"begin":1424,"end":1428},"obj":"OrganismTaxon"},{"id":"T11","span":{"begin":1487,"end":1491},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"10088"},{"id":"A2","pred":"db_id","subj":"T2","obj":"10088"},{"id":"A3","pred":"db_id","subj":"T3","obj":"10088"},{"id":"A4","pred":"db_id","subj":"T4","obj":"10088"},{"id":"A5","pred":"db_id","subj":"T5","obj":"10088"},{"id":"A6","pred":"db_id","subj":"T6","obj":"10088"},{"id":"A7","pred":"db_id","subj":"T7","obj":"10088"},{"id":"A8","pred":"db_id","subj":"T8","obj":"10088"},{"id":"A9","pred":"db_id","subj":"T9","obj":"10088"},{"id":"A10","pred":"db_id","subj":"T10","obj":"10088"},{"id":"A11","pred":"db_id","subj":"T11","obj":"10088"}],"namespaces":[{"prefix":"_base","uri":"https://glycosmos.org/organisms/"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos15-CL

{"project":"GlyCosmos15-CL","denotations":[{"id":"T1","span":{"begin":390,"end":405},"obj":"Cell"},{"id":"T2","span":{"begin":653,"end":660},"obj":"Cell"},{"id":"T3","span":{"begin":825,"end":832},"obj":"Cell"},{"id":"T4","span":{"begin":974,"end":981},"obj":"Cell"},{"id":"T5","span":{"begin":1544,"end":1551},"obj":"Cell"},{"id":"T6","span":{"begin":1620,"end":1626},"obj":"Cell"},{"id":"T7","span":{"begin":1627,"end":1643},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000128"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A3","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A4","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A5","pred":"cl_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A6","pred":"cl_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A7","pred":"cl_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CL:0000115"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos15-UBERON

{"project":"GlyCosmos15-UBERON","denotations":[{"id":"T1","span":{"begin":383,"end":389},"obj":"Body_part"},{"id":"T2","span":{"begin":390,"end":405},"obj":"Body_part"},{"id":"T3","span":{"begin":1080,"end":1091},"obj":"Body_part"},{"id":"T4","span":{"begin":1177,"end":1181},"obj":"Body_part"},{"id":"T5","span":{"begin":1237,"end":1259},"obj":"Body_part"},{"id":"T6","span":{"begin":1261,"end":1264},"obj":"Body_part"},{"id":"T7","span":{"begin":1342,"end":1345},"obj":"Body_part"},{"id":"T8","span":{"begin":1561,"end":1564},"obj":"Body_part"},{"id":"T9","span":{"begin":1620,"end":1626},"obj":"Body_part"},{"id":"T10","span":{"begin":1627,"end":1643},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000345"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL_0000128"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0001986"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0002398"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"A10","pred":"uberon_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/CL_0000115"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

sentences

GlyCosmos15-Sentences

{"project":"GlyCosmos15-Sentences","blocks":[{"id":"T1","span":{"begin":0,"end":94},"obj":"Sentence"},{"id":"T2","span":{"begin":95,"end":374},"obj":"Sentence"},{"id":"T3","span":{"begin":375,"end":441},"obj":"Sentence"},{"id":"T4","span":{"begin":442,"end":619},"obj":"Sentence"},{"id":"T5","span":{"begin":620,"end":778},"obj":"Sentence"},{"id":"T6","span":{"begin":779,"end":937},"obj":"Sentence"},{"id":"T7","span":{"begin":938,"end":1163},"obj":"Sentence"},{"id":"T8","span":{"begin":1164,"end":1429},"obj":"Sentence"},{"id":"T9","span":{"begin":1430,"end":1565},"obj":"Sentence"},{"id":"T10","span":{"begin":1566,"end":1691},"obj":"Sentence"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos15-GlycoEpitope

{"project":"GlyCosmos15-GlycoEpitope","denotations":[{"id":"T1","span":{"begin":256,"end":259},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T2","span":{"begin":261,"end":265},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T3","span":{"begin":267,"end":271},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T4","span":{"begin":273,"end":277},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T5","span":{"begin":283,"end":287},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"}],"attributes":[{"id":"A1","pred":"glycoepitope_id","subj":"T1","obj":"http://www.glycoepitope.jp/epitopes/EP0050"},{"id":"A2","pred":"glycoepitope_id","subj":"T2","obj":"http://www.glycoepitope.jp/epitopes/EP0056"},{"id":"A3","pred":"glycoepitope_id","subj":"T3","obj":"http://www.glycoepitope.jp/epitopes/EP0059"},{"id":"A4","pred":"glycoepitope_id","subj":"T4","obj":"http://www.glycoepitope.jp/epitopes/EP0067"},{"id":"A5","pred":"glycoepitope_id","subj":"T5","obj":"http://www.glycoepitope.jp/epitopes/EP0069"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos15-FMA

{"project":"GlyCosmos15-FMA","denotations":[{"id":"T1","span":{"begin":390,"end":405},"obj":"Body_part"},{"id":"T2","span":{"begin":999,"end":1023},"obj":"Body_part"},{"id":"T3","span":{"begin":1080,"end":1091},"obj":"Body_part"},{"id":"T4","span":{"begin":1177,"end":1181},"obj":"Body_part"},{"id":"T5","span":{"begin":1237,"end":1259},"obj":"Body_part"},{"id":"T6","span":{"begin":1261,"end":1264},"obj":"Body_part"},{"id":"T7","span":{"begin":1342,"end":1345},"obj":"Body_part"},{"id":"T8","span":{"begin":1561,"end":1564},"obj":"Body_part"},{"id":"T9","span":{"begin":1627,"end":1643},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"FMA:54540"},{"id":"A2","pred":"db_id","subj":"T2","obj":"FMA:273565"},{"id":"A3","pred":"db_id","subj":"T3","obj":"FMA:63916"},{"id":"A4","pred":"db_id","subj":"T4","obj":"FMA:9712"},{"id":"A5","pred":"db_id","subj":"T5","obj":"FMA:55675"},{"id":"A6","pred":"db_id","subj":"T6","obj":"FMA:55675"},{"id":"A7","pred":"db_id","subj":"T7","obj":"FMA:55675"},{"id":"A8","pred":"db_id","subj":"T8","obj":"FMA:55675"},{"id":"A9","pred":"db_id","subj":"T9","obj":"FMA:66772"}],"namespaces":[{"prefix":"FMA","uri":"http://purl.org/sig/ont/fma/fma"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos15-MAT

{"project":"GlyCosmos15-MAT","denotations":[{"id":"T1","span":{"begin":1177,"end":1181},"obj":"Body_part"},{"id":"T2","span":{"begin":1237,"end":1259},"obj":"Body_part"},{"id":"T3","span":{"begin":1261,"end":1264},"obj":"Body_part"},{"id":"T4","span":{"begin":1342,"end":1345},"obj":"Body_part"},{"id":"T5","span":{"begin":1561,"end":1564},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000091"},{"id":"A2","pred":"mat_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"A3","pred":"mat_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"A4","pred":"mat_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MAT_0000457"},{"id":"A5","pred":"mat_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MAT_0000457"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos15-Glycan

NCBITAXON

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":183,"end":187},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":614,"end":618},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":690,"end":694},"obj":"OrganismTaxon"},{"id":"T4","span":{"begin":708,"end":712},"obj":"OrganismTaxon"},{"id":"T5","span":{"begin":848,"end":852},"obj":"OrganismTaxon"},{"id":"T6","span":{"begin":883,"end":887},"obj":"OrganismTaxon"},{"id":"T7","span":{"begin":920,"end":924},"obj":"OrganismTaxon"},{"id":"T8","span":{"begin":1158,"end":1162},"obj":"OrganismTaxon"},{"id":"T9","span":{"begin":1371,"end":1375},"obj":"OrganismTaxon"},{"id":"T10","span":{"begin":1424,"end":1428},"obj":"OrganismTaxon"},{"id":"T11","span":{"begin":1487,"end":1491},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"10088"},{"id":"A2","pred":"db_id","subj":"T2","obj":"10088"},{"id":"A3","pred":"db_id","subj":"T3","obj":"10088"},{"id":"A4","pred":"db_id","subj":"T4","obj":"10088"},{"id":"A5","pred":"db_id","subj":"T5","obj":"10088"},{"id":"A6","pred":"db_id","subj":"T6","obj":"10088"},{"id":"A7","pred":"db_id","subj":"T7","obj":"10088"},{"id":"A8","pred":"db_id","subj":"T8","obj":"10088"},{"id":"A9","pred":"db_id","subj":"T9","obj":"10088"},{"id":"A10","pred":"db_id","subj":"T10","obj":"10088"},{"id":"A11","pred":"db_id","subj":"T11","obj":"10088"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

GlyCosmos-GlycoEpitope

{"project":"GlyCosmos-GlycoEpitope","denotations":[{"id":"T1","span":{"begin":256,"end":259},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T2","span":{"begin":261,"end":265},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T3","span":{"begin":267,"end":271},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T4","span":{"begin":273,"end":277},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T5","span":{"begin":283,"end":287},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"}],"attributes":[{"id":"A1","pred":"glycoepitope_id","subj":"T1","obj":"http://www.glycoepitope.jp/epitopes/EP0050"},{"id":"A2","pred":"glycoepitope_id","subj":"T2","obj":"http://www.glycoepitope.jp/epitopes/EP0056"},{"id":"A3","pred":"glycoepitope_id","subj":"T3","obj":"http://www.glycoepitope.jp/epitopes/EP0059"},{"id":"A4","pred":"glycoepitope_id","subj":"T4","obj":"http://www.glycoepitope.jp/epitopes/EP0067"},{"id":"A5","pred":"glycoepitope_id","subj":"T5","obj":"http://www.glycoepitope.jp/epitopes/EP0069"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

Anatomy-UBERON

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":383,"end":389},"obj":"Body_part"},{"id":"T2","span":{"begin":390,"end":405},"obj":"Body_part"},{"id":"T3","span":{"begin":1080,"end":1091},"obj":"Body_part"},{"id":"T4","span":{"begin":1177,"end":1181},"obj":"Body_part"},{"id":"T5","span":{"begin":1237,"end":1259},"obj":"Body_part"},{"id":"T6","span":{"begin":1261,"end":1264},"obj":"Body_part"},{"id":"T7","span":{"begin":1342,"end":1345},"obj":"Body_part"},{"id":"T8","span":{"begin":1561,"end":1564},"obj":"Body_part"},{"id":"T9","span":{"begin":1620,"end":1626},"obj":"Body_part"},{"id":"T10","span":{"begin":1627,"end":1643},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000345"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL_0000128"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0001986"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0002398"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0001017"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"A10","pred":"uberon_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/CL_0000115"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}

CL-cell

{"project":"CL-cell","denotations":[{"id":"T1","span":{"begin":390,"end":405},"obj":"Cell"},{"id":"T2","span":{"begin":653,"end":660},"obj":"Cell"},{"id":"T3","span":{"begin":825,"end":832},"obj":"Cell"},{"id":"T4","span":{"begin":974,"end":981},"obj":"Cell"},{"id":"T5","span":{"begin":1544,"end":1551},"obj":"Cell"},{"id":"T6","span":{"begin":1620,"end":1626},"obj":"Cell"},{"id":"T7","span":{"begin":1627,"end":1643},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000128"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A3","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A4","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A5","pred":"cl_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A6","pred":"cl_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A7","pred":"cl_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CL:0000115"}],"text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of EAE."}