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http://purl.uniprot.org/citations/29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29770132http://www.w3.org/2000/01/rdf-schema#comment"gp130 cytokines are differentially involved in regulating the T helper (H) 17-driven pathogenesis of experimental autoimmune encephalomyelitis (EAE), the animal model of human multiple sclerosis. Interleukin (IL)-6 directly promotes the development of TH17 cells through the gp130/IL-6R complex. By contrast, IL-27 has been shown to suppress a TH17 immune response by gp130/IL-27R-alpha (α) receptor ligation. The IL-27-dependent regulation of a TH17 development could be mediated on the level of CD4 T cells. However, because IL-27 also suppresses the secretion of the TH17-driving cytokines IL-6 and IL-12/23p40 in accessory cells, TH17 immune responses may also be controlled by IL-27 on the level of macrophages and/or neutrophils. To analyze these opposing effects of gp130 engagement on the pathogenesis of EAE, we immunized CD4+ T cell-specific gp130-deficient (CD4creposgp130loxP/loxP) and macrophage/neutrophil-specific gp130-deficient (LysMcreposgp130loxP/loxP) mice with the myelin-oligodendrocyte-glycoprotein peptide MOG35-55. Whereas inflammatory immune responses, TH17 differentiation, and pathology in CD4creposgp130loxP/loxP mice were mitigated, disease progression was eventually enhanced in LysMcreposgp130loxP/loxP mice. Exacerbated disease in MOG35-55-immunized LysMcreposgp130loxP/loxP mice was associated with an elevated development of TH17 cells and increased infiltration of the central nervous system with leukocytes indicating a suppressive role of macrophage/neutrophil-gp130. To further prove IL-6 to be responsible for the control of inflammation during EAE through gp130 on macrophages/neutrophils, we immunized LysMcreposIL-6RloxP/loxP mice. In contrast to LysMcreposgp130loxP/loxP mice, neuropathology in MOG35-55-immunized macrophage/neutrophil-specific IL-6R-deficient mice was not enhanced indicating that the alleviation of EAE through macrophage/neutrophil-gp130 is mediated independently of IL-6. Together, this different pathology in macrophage/neutrophil- and CD4 T cell-specific gp130-deficient mice suggests that gp130 cytokines modulate TH17 inflammation differentially by targeting distinct cell types."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.org/dc/terms/identifier"doi:10.3389/fimmu.2018.00836"xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Deng F."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Rose-John S."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Prinz M."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Holscher C."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Holscher A."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Holz K."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Brendecke S.M."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/author"Mitrucker H.W."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/name"Front Immunol"xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/pages"836"xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/title"Differing Outcome of Experimental Autoimmune Encephalitis in Macrophage/Neutrophil- and T Cell-Specific gp130-Deficient Mice."xsd:string
http://purl.uniprot.org/citations/29770132http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/29770132http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29770132
http://purl.uniprot.org/citations/29770132http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29770132
http://purl.uniprot.org/uniprot/#_A0A0G2JGF1-mappedCitation-29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29770132
http://purl.uniprot.org/uniprot/#_A0A077S2U6-mappedCitation-29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29770132
http://purl.uniprot.org/uniprot/#_H6WCS3-mappedCitation-29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29770132
http://purl.uniprot.org/uniprot/#_Q3UQA0-mappedCitation-29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29770132
http://purl.uniprot.org/uniprot/#_P22272-mappedCitation-29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29770132
http://purl.uniprot.org/uniprot/#_Q6PDI9-mappedCitation-29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29770132
http://purl.uniprot.org/uniprot/#_P08905-mappedCitation-29770132http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29770132