دورية أكاديمية
أعرض في EDS

Oligodendrocytes modulate the immune-inflammatory response in EAE via TNFR2 signaling.

التفاصيل البيبلوغرافية
العنوان: Oligodendrocytes modulate the immune-inflammatory response in EAE via TNFR2 signaling.
المؤلفون: Madsen PM; The Miami Project to Cure Paralysis, Dept. Neurological Surgery, University of Miami Miller School of Medicine, FL 33136, USA; Dept. Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark., Desu HL; The Miami Project to Cure Paralysis, Dept. Neurological Surgery, University of Miami Miller School of Medicine, FL 33136, USA; The Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA., de Rivero Vaccari JP; The Miami Project to Cure Paralysis, Dept. Neurological Surgery, University of Miami Miller School of Medicine, FL 33136, USA., Florimon Y; The Miami Project to Cure Paralysis, Dept. Neurological Surgery, University of Miami Miller School of Medicine, FL 33136, USA., Ellman DG; Dept. Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark., Keane RW; The Miami Project to Cure Paralysis, Dept. Neurological Surgery, University of Miami Miller School of Medicine, FL 33136, USA; The Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA; Dept. Physiology and Biophysics, University of Miami Miller School of Medicine, FL 33136, USA., Clausen BH; Dept. Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark; BRIDGE - Brain Research Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, Odense, Denmark., Lambertsen KL; Dept. Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark; Department of Neurology, Odense University Hospital, Odense, Denmark; BRIDGE - Brain Research Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, Odense, Denmark., Brambilla R; The Miami Project to Cure Paralysis, Dept. Neurological Surgery, University of Miami Miller School of Medicine, FL 33136, USA; Dept. Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark; The Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA; BRIDGE - Brain Research Inter Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Electronic address: r.brambilla@miami.edu.
المصدر: Brain, behavior, and immunity [Brain Behav Immun] 2020 Feb; Vol. 84, pp. 132-146. Date of Electronic Publication: 2019 Nov 27.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 8800478 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2139 (Electronic) Linking ISSN: 08891591 NLM ISO Abbreviation: Brain Behav Immun Subsets: MEDLINE
أسماء مطبوعة: Publication: <2000- > : Amsterdam : Elsevier
Original Publication: San Diego : Academic Press, [c1987-
مواضيع طبية MeSH: Signal Transduction*, Encephalomyelitis, Autoimmune, Experimental/*immunology , Encephalomyelitis, Autoimmune, Experimental/*pathology , Multiple Sclerosis/*immunology , Multiple Sclerosis/*pathology , Oligodendroglia/*immunology , Receptors, Tumor Necrosis Factor, Type II/*metabolism, Animals ; Female ; Mice ; Mice, Inbred C57BL
مستخلص: The pleotropic cytokine tumor necrosis factor (TNF) is involved in the pathophysiology of multiple sclerosis (MS). In various models of MS, including experimental autoimmune encephalomyelitis (EAE), the membrane-bound form of TNF (tmTNF), which signals primarily via TNFR2, mediates protective and reparative effects, whereas the soluble form (solTNF), which signals primarily via TNFR1, promotes pro-inflammatory and detrimental functions. In this study, we investigated the role of TNFR2 expressed in oligodendrocytes in the early phase of EAE pathogenesis. We demonstrated that mice with specific ablation of oligodendroglial TNFR2 displayed early onset and higher peak of motor dysfunction when subjected to EAE, in advance of which accelerated infiltration of immune cells was observed as early as 10 days post EAE induction. The immune cell influx was preceded by microglial activation and increased blood brain barrier permeability. Lack of oligodendroglial TNFR2 accelerated the expression of inflammatory cytokines as well as expression and activation of the inflammasome. Gene expression profiling of oligodendrocytes sorted from the spinal cord 14 days post EAE induction showed robust upregulation of inflammatory genes, some of which were elevated in cells lacking TNFR2 compared to controls. Together, our data demonstrate that oligodendrocytes are directly involved in inflammation and immune modulation in CNS disease and this function is regulated, at least in part, by TNFR2.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2019 Elsevier Inc. All rights reserved.)
التعليقات: Erratum in: Brain Behav Immun. 2021 Jul;95:520. (PMID: 33933332)
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معلومات مُعتمدة: R01 NS094522 United States NS NINDS NIH HHS
فهرسة مساهمة: Keywords: Cytokines; Demyelination; Multiple sclerosis; Neurodegeneration; Neuroinflammation; Oligodendrocytes; Tumor necrosis factor
المشرفين على المادة: 0 (Receptors, Tumor Necrosis Factor, Type II)
تواريخ الأحداث: Date Created: 20191201 Date Completed: 20210312 Latest Revision: 20210502
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC7010565
DOI: 10.1016/j.bbi.2019.11.017
PMID: 31785393
قاعدة البيانات: MEDLINE
الوصف
تدمد:1090-2139
DOI:10.1016/j.bbi.2019.11.017