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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP-
dc.contributor.authorKANEKO, Kimihiko-
dc.contributor.authorSATO, Douglas Kazutoshi-
dc.contributor.authorNAKASHIMA, Ichiro-
dc.contributor.authorOGAWA, Ryo-
dc.contributor.authorAKAISHI, Tetsuya-
dc.contributor.authorTAKAI, Yoshiki-
dc.contributor.authorNISHIYAMA, Shuhei-
dc.contributor.authorTAKAHASHI, Toshiyuki-
dc.contributor.authorMISU, Tatsuro-
dc.contributor.authorKURODA, Hiroshi-
dc.contributor.authorTANAKA, Satoru-
dc.contributor.authorNOMURA, Kyoichi-
dc.contributor.authorHASHIMOTO, Yuji-
dc.contributor.authorCALLEGARO, Dagoberto-
dc.contributor.authorSTEINMAN, Lawrence-
dc.contributor.authorFUJIHARA, Kazuo-
dc.contributor.authorAOKI, Masashi-
dc.identifier.citationJOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, v.89, n.9, p.927-936, 2018-
dc.description.abstractObjective To evaluate cerebrospinal fluid (CSF) cytokine profiles in myelin oligodendrocyte glycoprotein IgG-positive (MOG-IgG+) disease in adult and paediatric patients. Methods In this cross-sectional study, we measured 27 cytokines in the CSF of MOG-IgG+ disease in acute phase before treatment (n=29). The data were directly compared with those in aquaporin-4 antibody-positive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD) (n=20), multiple sclerosis (MS) (n=20) and non-inflammatory controls (n=14). Results In MOG-IgG+ disease, there was no female preponderance and the ages were younger (mean 18 years, range 3-68; 15 were below 18 years) relative to AQP4-IgG+ NMOSD (41, 15-77) and MS (34, 17-48). CSF cell counts were higher and oligoclonal IgG bands were mostly negative in MOG-IgG+ disease and AQP4-IgG+ NMOSD compared with MS. MOG-IgG+ disease had significantly elevated levels of interleukin (IL)-6, IL-8, granulocyte-colony stimulating factor and granulocyte macrophage-colony stimulating factor, interferon-gamma, IL-10, IL-1 receptor antagonist, monocyte chemotactic protein-1 and macrophage inflammatory protein-1 alpha as compared with MS. No cytokine in MOG-IgG+ disease was significantly different from AQP4-IgG+ NMOSD. Moreover many elevated cytokines were correlated with each other in MOG-IgG+ disease and AQP4-IgG+ NMOSD but not in MS. No difference in the data was seen between adult and paediatric MOG-IgG+ cases. Conclusions The CSF cytokine profile in the acute phase of MOG-IgG+ disease is characterised by coordinated upregulation of T helper 17 (Th17) and other cytokines including some Th1-related and regulatory T cells-related ones in adults and children, which is similar to AQP4-IgG+ NMOSD but clearly different from MS. The results suggest that as with AQP4-IgG+ NMOSD, some disease-modifying drugs for MS may be ineffective in MOG-IgG+ disease while they may provide potential therapeutic targets.-
dc.description.sponsorshipJapan Society for the Promotion of Science (KAKENHI)-
dc.description.sponsorshipHealth and Labour Sciences Research Grant on Intractable Diseases (neuroimmunological diseases) from the Ministry of Health, Labour and Welfare of Japan-
dc.relation.ispartofJournal of Neurology Neurosurgery and Psychiatry-
dc.subject.othermyelin-oligodendrocyte glycoprotein-
dc.subject.otherneuromyelitis-optica spectrum-
dc.subject.otherdemyelinating diseases-
dc.titleCSF cytokine profile in MOG-IgG plus neurological disease is similar to AQP4-IgG+ NMOSD but distinct from MS: a cross-sectional study and potential therapeutic implications-
dc.rights.holderCopyright BMJ PUBLISHING GROUP-
dc.subject.wosClinical Neurology-
dc.type.categoryoriginal article-
dc.type.versionpublishedVersion-, Kimihiko:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan-, Ichiro:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan; Tohoku Med & Pharmaceut Univ, Dept Neurol, Sendai, Miyagi, Japan-, Ryo:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan-, Tetsuya:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan; Yonezawa Natl Hosp, Dept Neurol, Yonezawa, Yamagata, Japan-, Yoshiki:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan-, Shuhei:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan-, Toshiyuki:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan; Yonezawa Natl Hosp, Dept Neurol, Yonezawa, Yamagata, Japan-, Tatsuro:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan-, Hiroshi:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan-, Satoru:Saitama Med Univ, Dept Neurol, Kawagoe, Saitama, Japan-, Kyoichi:Saitama Med Univ, Dept Neurol, Kawagoe, Saitama, Japan-, Yuji:Chiba Kaihin Municipal Hosp, Dept Pediat, Chiba, Japan-, Lawrence:Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA-, Kazuo:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan; Fukushima Med Univ, Dept Multiple Sclerosis Therapeut, Fukushima, Japan; Tohoku Res Inst Neurosci, Multiple Sclerosis & Neuromyelitis Opt Ctr, Koriyama, Fukushima, Japan-, Masashi:Tohoku Univ, Grad Sch Med, Dept Neurol, Sendai, Miyagi, Japan-
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Instituto Central - HC/ICHC

Artigos e Materiais de Revistas Científicas - LIM/45
LIM/45 - Laboratório de Fisiopatologia Neurocirúrgica

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