Wrzos, Claudia

[["dc.bibliographiccitation.firstpage","768"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Annals of clinical and translational neurology"],["dc.bibliographiccitation.lastpage","783"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Malviya, Manish"],["dc.contributor.author","Barman, Sumanta"],["dc.contributor.author","Golombeck, Kristin S."],["dc.contributor.author","Planagumà, Jesús"],["dc.contributor.author","Mannara, Francesco"],["dc.contributor.author","Strutz-Seebohm, Nathalie"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Demir, Fatih"],["dc.contributor.author","Baksmeier, Christine"],["dc.contributor.author","Steckel, Julia"],["dc.contributor.author","Falk, Kim Kristin"],["dc.contributor.author","Gross, Catharina C."],["dc.contributor.author","Kovac, Stjepana"],["dc.contributor.author","Bönte, Kathrin"],["dc.contributor.author","Johnen, Andreas"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Martín-García, Elena"],["dc.contributor.author","Becker, Albert J."],["dc.contributor.author","Elger, Christian E."],["dc.contributor.author","Klöcker, Nikolaj"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Meuth, Sven G."],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Seebohm, Guiscard"],["dc.contributor.author","Leypoldt, Frank"],["dc.contributor.author","Maldonado, Rafael"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Dalmau, Josep"],["dc.contributor.author","Melzer, Nico"],["dc.contributor.author","Goebels, Norbert"],["dc.date.accessioned","2019-07-09T11:44:45Z"],["dc.date.available","2019-07-09T11:44:45Z"],["dc.date.issued","2017-11"],["dc.description.abstract","Objective: Autoimmune encephalitis is most frequently associated with anti-NMDAR autoantibodies. Their pathogenic relevance has been suggested by passive transfer of patients' cerebrospinal fluid (CSF) in mice in vivo. We aimed to analyze the intrathecal plasma cell repertoire, identify autoantibody-producing clones, and characterize their antibody signatures in recombinant form. Methods: Patients with recent onset typical anti-NMDAR encephalitis were subjected to flow cytometry analysis of the peripheral and intrathecal immune response before, during, and after immunotherapy. Recombinant human monoclonal antibodies (rhuMab) were cloned and expressed from matching immunoglobulin heavy- (IgH) and light-chain (IgL) amplicons of clonally expanded intrathecal plasma cells (cePc) and tested for their pathogenic relevance. Results: Intrathecal accumulation of B and plasma cells corresponded to the clinical course. The presence of cePc with hypermutated antigen receptors indicated an antigen-driven intrathecal immune response. Consistently, a single recombinant human GluN1-specific monoclonal antibody, rebuilt from intrathecal cePc, was sufficient to reproduce NMDAR epitope specificity in vitro. After intraventricular infusion in mice, it accumulated in the hippocampus, decreased synaptic NMDAR density, and caused severe reversible memory impairment, a key pathogenic feature of the human disease, in vivo. Interpretation: A CNS-specific humoral immune response is present in anti-NMDAR encephalitis specifically targeting the GluN1 subunit of the NMDAR. Using reverse genetics, we recovered the typical intrathecal antibody signature in recombinant form, and proved its pathogenic relevance by passive transfer of disease symptoms from man to mouse, providing the critical link between intrathecal immune response and the pathogenesis of anti-NMDAR encephalitis as a humorally mediated autoimmune disease."],["dc.identifier.doi","10.1002/acn3.444"],["dc.identifier.pmid","29159189"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59083"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2328-9503"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","NMDAR encephalitis: passive transfer from man to mouse by a recombinant antibody."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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","2678"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","2688"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Tammer, Roland"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2017-09-07T11:44:51Z"],["dc.date.available","2017-09-07T11:44:51Z"],["dc.date.issued","2011"],["dc.description.abstract","Magnetic resonance imaging (MRI) is the gold standard for the detection of multiple sclerosis (MS) lesions. However, current MRI techniques provide little information about the structural features of a brain lesion with inflammatory cell infiltration, demyelination, gliosis, acute axonal damage and axonal loss. To identify methods for a differentiation of demyelination, inflammation, and axonal damage we developed a novel mouse model combining cuprizone-induced demyelination and experimental autoimmune encephalomyelitis. MS-like brain lesions were assessed by T1-weighted, T2-weighted, and magnetization transfer MRI as well as by diffusion tensor imaging (DTI). T2-weighted MRI differentiated control and diseased mice, while T1-weighted MRI better reflected the extent of inflammation and axonal damage. In DTI, axonal damage and cellular infiltration led to a reduction of the axial diffusivity, whereas primary demyelination after cuprizone treatment was reflected by changes in radial but not axial diffusivity. Importantly, alterations in radial diffusivity were less pronounced in mice with demyelination, inflammation, and acute axonal damage, indicating that radial diffusivity may underestimate demyelination in acute MS lesions. In conclusion, the combined information from different DTI parameters allows for a more precise identification of solely demyelinated lesions versus demyelinated and acutely inflamed lesions. These findings are of relevance for offering individualized, stage-adapted therapies for MS patients."],["dc.identifier.doi","10.1016/j.neuroimage.2011.08.051"],["dc.identifier.gro","3150360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7115"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1053-8119"],["dc.title","Assessment of lesion pathology in a new animal model of MS by multiparametric MRI and DTI"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T08:51:35Z"],["dc.date.available","2018-11-07T08:51:35Z"],["dc.date.issued","2011"],["dc.format.extent","S154"],["dc.identifier.isi","000294178900605"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21968"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.issn","0894-1491"],["dc.title","TISSUE DAMAGE AND REPAIR AFTER SELECTIVE ASTROCYTE DEPLETION IN VIVO"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:05:36Z"],["dc.date.available","2018-11-07T09:05:36Z"],["dc.date.issued","2012"],["dc.format.extent","127"],["dc.identifier.isi","000328702200244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25360"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","Lyon, FRANCE"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Protection of oligodendroglia in experimental NMO lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","523"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","538"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Kayser, Dieter M."],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:42:12Z"],["dc.date.available","2018-11-07T09:42:12Z"],["dc.date.issued","2014"],["dc.description.abstract","Neuromyelitis optica (NMO) is a chronic, mostly relapsing inflammatory demyelinating disease of the CNS characterized by serum anti-aquaporin 4 (AQP4) antibodies in the majority of patients. Anti-AQP4 antibodies derived from NMO patients target and deplete astrocytes in experimental models when co-injected with complement. However, the time course and mechanisms of oligodendrocyte loss and demyelination and the fate of oligodendrocyte precursor cells (OPC) have not been examined in detail. Also, no studies regarding astrocyte repopulation of experimental NMO lesions have been reported. We utilized two rat models using either systemic transfer or focal intracerebral injection of recombinant human anti-AQP4 antibodies to generate NMO-like lesions. Time-course experiments were performed to examine oligodendroglial and astroglial damage and repair. In addition, oligodendrocyte pathology was studied in early human NMO lesions. Apart from early complement-mediated astrocyte destruction, we observed a prominent, very early loss of oligodendrocytes and oligodendrocyte precursor cells (OPCs) as well as a delayed loss of myelin. Astrocyte repopulation of focal NMO lesions was already substantial after 1 week. Olig2-positive OPCs reappeared before NogoA-positive, mature oligodendrocytes. Thus, using two experimental models that closely mimic the human disease, our study demonstrates that oligodendrocyte and OPC loss is an extremely early feature in the formation of human and experimental NMO lesions and leads to subsequent, delayed demyelination, highlighting an important difference in the pathogenesis of MS and NMO."],["dc.identifier.doi","10.1007/s00401-013-1220-8"],["dc.identifier.isi","000332957400005"],["dc.identifier.pmid","24292009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33902"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Early loss of oligodendrocytes in human and experimental neuromyelitis optica lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1196"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1209"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Bergner, Caroline G."],["dc.contributor.author","Meer, Franziska"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Türkmen, Mevlude"],["dc.contributor.author","Valizada, Emil"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2022-03-01T11:45:41Z"],["dc.date.available","2022-03-01T11:45:41Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/glia.23598"],["dc.identifier.eissn","1098-1136"],["dc.identifier.issn","0894-1491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103412"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Microglia damage precedes major myelin breakdown in X‐linked adrenoleukodystrophy and metachromatic leukodystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","eaam7816"],["dc.bibliographiccitation.issue","419"],["dc.bibliographiccitation.journal","Science Translational Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Fard, Maryam K."],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Sánchez, Paula"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Mandad, Sunit"],["dc.contributor.author","Jäkel, Sarah"],["dc.contributor.author","Fornasiero, Eugenio F."],["dc.contributor.author","Schmitt, Sebastian"],["dc.contributor.author","Ehrlich, Marc"],["dc.contributor.author","Starost, Laura"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Sergiou, Christina"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Dimou, Leda"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2020-12-10T18:36:46Z"],["dc.date.available","2020-12-10T18:36:46Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1126/scitranslmed.aam7816"],["dc.identifier.eissn","1946-6242"],["dc.identifier.issn","1946-6234"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76735"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","BCAS1 expression defines a population of early myelinating oligodendrocytes in multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","314"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","322"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Romanelli, Elisa"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Enz, Lukas"],["dc.contributor.author","Goebels, Norbert"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T10:11:38Z"],["dc.date.available","2018-11-07T10:11:38Z"],["dc.date.issued","2016"],["dc.description.abstract","Breakdown of myelin sheaths is a pathological hallmark of several autoimmune diseases of the nervous system. We employed autoantibody-mediated animal models of demyelinating diseases, including a rat model of neuromyelitis optica (NMO), to target myelin and found that myelin lamellae are broken down into vesicular structures at the innermost region of the myelin sheath. We demonstrated that myelin basic proteins (MBP), which form a polymer in between the myelin membrane layers, are targeted in these models. Elevation of intracellular Ca2+ levels resulted in MBP network disassembly and myelin vesiculation. We propose that the aberrant phase transition of MBP molecules from their cohesive to soluble and non-adhesive state is a mechanism triggering myelin breakdown in NMO and possibly in other demyelinating diseases."],["dc.identifier.doi","10.1016/j.celrep.2016.06.008"],["dc.identifier.isi","000380262300005"],["dc.identifier.pmid","27346352"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13675"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40088"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Loss of Myelin Basic Protein Function Triggers Myelin Breakdown in Models of Demyelinating Diseases"],["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.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","34"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Lagumersindez-Denis, Nielsen"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Hollasch, Heiko"],["dc.contributor.author","Flach, Anne"],["dc.contributor.author","Bruehl, Hilke"],["dc.contributor.author","Cullen, Eilish"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Linington, Christopher"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nessler, Stefan"],["dc.date.accessioned","2018-11-07T10:22:07Z"],["dc.date.available","2018-11-07T10:22:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Cortical demyelination is a widely recognized hallmark of multiple sclerosis (MS) and correlate of disease progression and cognitive decline. The pathomechanisms initiating and driving gray matter damage are only incompletely understood. Here, we determined the infiltrating leukocyte subpopulations in 26 cortical demyelinated lesions of biopsied MS patients and assessed their contribution to cortical lesion formation in a newly developed mouse model. We find that conformation-specific anti-myelin antibodies contribute to cortical demyelination even in the absence of the classical complement pathway. T cells and natural killer cells are relevant for intracortical type 2 but dispensable for subpial type 3 lesions, whereas CCR2(+) monocytes are required for both. Depleting CCR2(+) monocytes in marmoset monkeys with experimental autoimmune encephalomyelitis using a novel humanized CCR2 targeting antibody translates into significantly less cortical demyelination and disease severity. We conclude that biologics depleting CCR2(+) monocytes might be attractive candidates for preventing cortical lesion formation and ameliorating disease progression in MS."],["dc.identifier.doi","10.1007/s00401-017-1706-x"],["dc.identifier.isi","000403235900002"],["dc.identifier.pmid","28386765"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14713"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42218"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Differential contribution of immune effector mechanisms to cortical demyelination in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]