Institut für Neuroimmunologie und Multiple-Sklerose-Forschung

[["dc.bibliographiccitation.firstpage","117"],["dc.bibliographiccitation.lastpage","129"],["dc.contributor.author","Schläger, Christian"],["dc.contributor.author","Litke, Tanja"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.editor","Weissert, Robert"],["dc.date.accessioned","2020-07-06T13:57:37Z"],["dc.date.available","2020-07-06T13:57:37Z"],["dc.date.issued","2016"],["dc.description.abstract","The CNS is effectively shielded from the periphery by the blood-brain barrier (BBB) which limits the entry of cells and solutes. However, in autoimmune disorders such as multiple sclerosis, immune cells can overcome this barrier and induce the formation of CNS inflammatory lesions. Recently, two-photon laser scanning microscopy (TPLSM) has made it possible to visualize autoimmune processes in the living CNS in real time. However, along with a high microscopy standard, this technique requires an advanced surgical procedure to access the region of interest. Here, we describe in detail the necessary methodological steps to visualize (auto)immune processes in living rodent tissue. We focus on the procedures to image the leptomeningeal vessels of the thoracic spinal cord during transfer experimental autoimmune encephalomyelitis in LEW rats (AT EAE) and in active EAE in C57BL/6 mice (aEAE)."],["dc.identifier.doi","10.1007/7651_2014_150"],["dc.identifier.pmid","25549830"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66861"],["dc.language.iso","en"],["dc.publisher","Springer"],["dc.relation.ispartof","Multiple Sclerosis: Methods and Protocols"],["dc.title","In Vivo Visualization of (Auto)Immune Processes in the Central Nervous System of Rodents"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1805"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Experimental Medicine"],["dc.bibliographiccitation.lastpage","1814"],["dc.bibliographiccitation.volume","201"],["dc.contributor.author","Kawakami, Naoto"],["dc.contributor.author","Nägerl, U Valentin"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Bonhoeffer, Tobias"],["dc.contributor.author","Wekerle, Hartmut"],["dc.contributor.author","Flügel, Alexander"],["dc.date.accessioned","2020-07-06T13:58:17Z"],["dc.date.available","2020-07-06T13:58:17Z"],["dc.date.issued","2005-06-06"],["dc.description.abstract","We tracked pathogenic myelin basic protein-specific CD4+ effector T cells in early central nervous system (CNS) lesions of experimental autoimmune encephalomyelitis (EAE) by combining two-photon imaging and fluorescence video microscopy. We made two key observations: (a) the majority of the cells (65%) moved fast (maximal speed 25 microm/min) and apparently nondirected through the compact tissue; and (b) a second group of effector T cells (35%) appeared tethered to a fixed point. Polarization of T cell receptor and adhesion molecules (lymphocyte function-associated antigen 1) towards this fixed point suggests the formation of immune synapses. Nonpathogenic, ovalbumin-specific T cells were not tethered in the CNS and did not form synapse-like contacts, but moved through the tissue. After intrathecal injection of antigen, 40% of ovalbumin-specific T cells became tethered. Conversely, injection of anti-major histocompatibility complex class II antibodies profoundly reduced the number of stationary pathogenic T cells within the CNS (to 15%). We propose that rapid penetration of the CNS parenchyma by numerous autoimmune effector T cells along with multiple autoantigen-presentation events are responsible for the fulminate development of clinical EAE."],["dc.identifier.doi","10.1084/jem.20050011"],["dc.identifier.pmid","15939794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66867"],["dc.language.iso","en"],["dc.relation.issn","0022-1007"],["dc.title","Live imaging of effector cell trafficking and autoantigen recognition within the unfolding autoimmune encephalomyelitis lesion"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Gao, Ming"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Thal, Dietmar R."],["dc.contributor.author","Chang, Mayland"],["dc.contributor.author","Opdenakker, Ghislain"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2021-04-14T08:28:11Z"],["dc.date.available","2021-04-14T08:28:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1172/JCI141694"],["dc.identifier.pmid","33645550"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82526"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/22"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B02: Inflammatory neurodegeneration and repair mechanisms in childhood onset autoimmune and neurometabolic demyelinating CNS disease"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Blood-brain barrier resealing in neuromyelitis optica occurs independently of astrocyte regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","979"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Immunobiology"],["dc.bibliographiccitation.lastpage","987"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Miljkovic, Djordje"],["dc.contributor.author","Stanojevic, Zeljka"],["dc.contributor.author","Momcilovic, Miljana"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Mostarica-Stojkovic, Marija"],["dc.date.accessioned","2018-11-07T08:52:09Z"],["dc.date.available","2018-11-07T08:52:09Z"],["dc.date.issued","2011"],["dc.description.abstract","Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis, a chronic inflammatory and demyelinating disease of the CNS. Albino Oxford (AO) rats are resistant to the induction of EAE, while the disease can be readily induced in Dark Agouti (DA) rats. Here we investigated a potential contribution of the CNS milieu in the limitation of the encephalitogenic autoimmune response. EAE was induced by immunization of the respective rat strains with spinal cord homogenate emulsified in complete Freund's adjuvant. AO rats did not exhibit clinical signs after immunization while DA rats developed severe neurologic deficits. Infiltration of immune cells into spinal cords (SC) was evident in both strains 12-14 days after the immunization. EAE lesions of AO rats contained substantially lower numbers of CD4+ T cells and CD11b+ cells compared to those in DA rats. This went together with lower levels of interferon (IFN)-gamma and interleukin (IL)-17 in the cells isolated from SC. We found a dramatic increase of CXCL12 expression in SC tissue and microvessels of AO rats, whereas DA rats markedly decreased the expression of this chemokine within their CNS. Administration of the CXCL12 antagonist AMD3100 to a substrain of AO rats that developed a weak EAE led to earlier onset and exacerbation of the disease. These results suggest a role of CXCL12 in down-regulating autoimmune processes in AO rats during EAE. Therapeutic modulation of CXCL12 could be a promising strategy for the treatment of CNS autoimmunity. (C) 2011 Elsevier GmbH. All rights reserved."],["dc.identifier.doi","10.1016/j.imbio.2011.03.013"],["dc.identifier.isi","000295606600002"],["dc.identifier.pmid","21601937"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22101"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.relation.issn","0171-2985"],["dc.title","CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","60"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Spieth, Lena"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Schlaphoff, Lennart"],["dc.contributor.author","Depp, Constanze"],["dc.contributor.author","Düking, Tim"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Neuber, Jonathan"],["dc.contributor.author","Ewers, David"],["dc.contributor.author","Scholz, Patricia"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Sasmita, Andrew O."],["dc.contributor.author","Meschkat, Martin"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Sankowski, Roman"],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Huitinga, Inge"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Ischebeck, Till"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2021-04-14T08:27:05Z"],["dc.date.available","2021-04-14T08:27:05Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41593-020-00757-6"],["dc.identifier.pmid","33349711"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82162"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/11"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A04: The role of the meninges in the resolution of acute autoimmune CNS lesions"],["dc.relation.eissn","1546-1726"],["dc.relation.issn","1097-6256"],["dc.relation.workinggroup","RG Cantuti"],["dc.relation.workinggroup","RG Nave (Neurogenetics)"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.relation.workinggroup","RG Simons (The Biology of Glia in Development and Disease)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Microglia facilitate repair of demyelinated lesions via post-squalene sterol synthesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","105"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","118"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Puchert, Malte"],["dc.contributor.author","Pelkner, Fabian"],["dc.contributor.author","Stein, Gregor"],["dc.contributor.author","Angelov, Doychin N"],["dc.contributor.author","Boltze, Johannes"],["dc.contributor.author","Wagner, Daniel-Christoph"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Streit, Wolfgang J"],["dc.contributor.author","Engele, Jürgen"],["dc.date.accessioned","2020-07-06T13:57:26Z"],["dc.date.available","2020-07-06T13:57:26Z"],["dc.date.issued","2017"],["dc.description.abstract","Based on our previous demonstration of CXCR7 as the major mediator of CXCL12 signaling in cultured astrocytes, we have now compared astrocytic expression of the CXCL12 receptors, CXCR7 and CXCR4, during CNS development and disease. In addition, we asked whether disease-associated conditions/factors affect expression of CXCL12 receptors in astrocytes. In the late embryonic rat brain, CXCR7+/GFAP+ cells were restricted to the ventricular/subventricular zone while CXCR4 was widely absent from GFAP-positive cells. In the early postnatal and adult brain, CXCR7 and CXCR4 were almost exclusively expressed by GFAP-immunoreactive astrocytes forming the superficial glia limitans. Contrasting the situation in the intact CNS, a striking increase in astrocytic CXCR7 expression was detectable in the cortex of rats with experimental brain infarcts, in the spinal cord of rats with experimental autoimmune encephalomyelitis (EAE) and after mechanical compression, as well as in the in infarcted human cerebral cortex and in the hippocampus of Alzheimer's disease patients. None of these pathologies was associated with substantial increases in astrocytic CXCR4 expression. Screening of various disease-associated factors/conditions further revealed that CXCR7 expression of cultured cortical astrocytes increases with IFNγ as well as under hypoxic conditions whereas CXCR7 expression is attenuated following treatment with IFNβ. Again, none of the treatments affected CXCR4 expression in cultured astrocytes. Together, these findings support the hypothesis of a crucial role of astrocytic CXCR7 in the progression of various CNS pathologies."],["dc.identifier.doi","10.1016/j.mcn.2017.09.001"],["dc.identifier.pmid","28889992"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66859"],["dc.language.iso","en"],["dc.relation.eissn","1095-9327"],["dc.relation.issn","1044-7431"],["dc.title","Astrocytic expression of the CXCL12 receptor, CXCR7/ACKR3 is a hallmark of the diseased, but not developing CNS"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","69"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","81"],["dc.bibliographiccitation.volume","175"],["dc.contributor.author","Kawakami, Naoto"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.contributor.author","Bradl, Monika"],["dc.contributor.author","Ritter, Thomas"],["dc.contributor.author","Neuhaus, Oliver"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Wekerle, Hartmut"],["dc.contributor.author","Flügel, Alexander"],["dc.date.accessioned","2020-07-06T13:58:28Z"],["dc.date.available","2020-07-06T13:58:28Z"],["dc.date.issued","2005-07-01"],["dc.description.abstract","We embedded green fluorescent CD4(+) T cells specific for myelin basic protein (MBP) (T(MBP-GFP) cells) in the immune system of syngeneic neonatal rats. These cells persisted in the animals for the entire observation period spanning >2 years without affecting the health of the hosts. They maintained a memory phenotype with low levels of L-selectin and CD45RC, but high CD44. Although persisting in low numbers (0.01-0.1% of lymph node cells) they were sufficient to raise susceptibility toward clinical autoimmune disease. Immunization with MBP in IFA induced CNS inflammation and overt clinical disease in animals carrying neonatally transferred T(MBP-GFP) cells, but not in controls. The onset of the clinical disease coincided with mass infiltration of T(MBP-GFP) cells into the CNS. In the periphery, following the amplification phase a rapid contraction of the T cell population was observed. However, elevated numbers of fully reactive T(MBP-GFP) cells remained in the peripheral immune system after acute experimental autoimmune encephalomyelitis mediating reimmunization-induced disease relapses."],["dc.identifier.doi","10.4049/jimmunol.175.1.69"],["dc.identifier.pmid","15972633"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66869"],["dc.language.iso","en"],["dc.relation.issn","0022-1767"],["dc.title","Autoimmune CD4+ T cell memory: lifelong persistence of encephalitogenic T cell clones in healthy immune repertoires"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Lodygin, Dmitri"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Koerner, Henrike"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger"],["dc.contributor.author","Kitz, Alexandra"],["dc.contributor.author","Nosov, Michail"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:02:16Z"],["dc.date.available","2018-11-07T09:02:16Z"],["dc.date.issued","2012"],["dc.identifier.isi","000312764800352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24643"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Boston, MA"],["dc.title","Direct imaging of T cell activation during experimental autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1405"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","1416"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Mueller, Nora"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Herath, Judith"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T11:16:37Z"],["dc.date.available","2018-11-07T11:16:37Z"],["dc.date.issued","2008"],["dc.description.abstract","Administration of the CD28 superagonistic antibody JJ316 is an efficient means to treat autoimmune diseases in rats, but the humanized antibody TGN1412 caused devastating side effects in healthy volunteers during a clinical trial. Here we show that JJ316 treatment of rats induced a dramatic redistribution of T lymphocytes from the periphery to the secondary lymphoid organs, resulting in severe T lymphopenia. Live imaging of secondary lymphoid organs revealed that JJ316 administration almost instantaneously (<2 minutes) arrested T cells in situ. This reduction in T cell motility was accompanied by profound cytoskeletal rearrangements and increased cell size. In addition, surface expression of lymphocyte function-associated antigen-1 was enhanced, endothelial differentiation sphingolipid G protein-coupled receptor 1 and L selectin levels were downregulated, and the cells lost their responsiveness to sphingosine 1-phosphate-directed migration. These proadhesive alterations were accompanied by signs of strong activation, including upregulation of CD25, CD69, CD134, and proinflammatory mediators. However, this did not lead to a cytokine storm similar to the clinical trial. While most of the early changes disappeared within 48 hours, we observed that CD4(+)CD25(+)FoxP3(+) regulatory T cells experienced a second phase of activation, which resulted in massive cell enlargement, extensive polarization, and increased motility. These data suggest that CD28 superagonists elicit 2 qualitatively distinct waves of activation."],["dc.identifier.doi","10.1172/JCI32698"],["dc.identifier.isi","000254588600034"],["dc.identifier.pmid","18357346"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6254"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54633"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Investigation Inc"],["dc.relation.issn","0021-9738"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A CD28 superagonistic antibody elicits 2 functionally distinct waves of T cell activation in rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14241"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Gerndt, Nina"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Stumpf, Sina Kristin"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Boehler, Carolin"],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Stassart, Ruth"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2018-11-07T10:28:16Z"],["dc.date.available","2018-11-07T10:28:16Z"],["dc.date.issued","2017"],["dc.description.abstract","Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure contributes to persistent disability. Cholesterol is rate-limiting for myelin biogenesis in the developing CNS; however, whether cholesterol insufficiency contributes to remyelination failure in MS, is unclear. Here, we show the relationship between cholesterol, myelination and neurological parameters in mouse models of demyelination and remyelination. In the cuprizone model, acute disease reduces serum cholesterol levels that can be restored by dietary cholesterol. Concomitant with blood-brain barrier impairment, supplemented cholesterol directly supports oligodendrocyte precursor proliferation and differentiation, and restores the balance of growth factors, creating a permissive environment for repair. This leads to attenuated axon damage, enhanced remyelination and improved motor learning. Remarkably, in experimental autoimmune encephalomyelitis, cholesterol supplementation does not exacerbate disease expression. These findings emphasize the safety of dietary cholesterol in inflammatory diseases and point to a previously unrecognized role of cholesterol in promoting repair after demyelinating episodes."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [SA 2014/2-1]; ERC Advanced grant"],["dc.identifier.doi","10.1038/ncomms14241"],["dc.identifier.isi","000392582700001"],["dc.identifier.pmid","28117328"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43386"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Dietary cholesterol promotes repair of demyelinated lesions in the adult brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]