Nessler, Stefan

[["dc.bibliographiccitation.firstpage","19057"],["dc.bibliographiccitation.issue","50"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","19062"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Zhou, D."],["dc.contributor.author","Srivastava, Rajneesh"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Grummel, Verena"],["dc.contributor.author","Sommer, Norbert"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T08:51:00Z"],["dc.date.available","2018-11-07T08:51:00Z"],["dc.date.issued","2006"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Although the cause of MS is still uncertain, many findings point toward an ongoing autoimmune response to myelin antigens. Because of its location on the outer surface of the myelin sheath and its pathogenicity in the experimental autoimmune encephalomyelitis model, myelin oligodendrocyte glycoprotein (MOG) is one of the potential disease-causing self antigens in MS. However, the role of MOG in the pathogenesis of MS has remained controversial. In this study we addressed the occurrence of autoantibodies to native MOG and its implication for demyelination and axonal loss in MS. We applied a high-sensitivity bioassay, which allowed detecting autoantibodies that bind to the extracellular part of native MOG. Antibodies, mostly IgG, were found in sera that bound with high affinity to strictly conformational epitopes of the extracellular domain of MOG. IgG but not IgM antibody titers to native MOG were significantly higher in MS patients compared with different control groups with the highest prevalence in primary progressive MS patients. Serum autoantibodies to native MOG induced death of MOG-expressing target cells in vitro. Serum from MS patients with high anti-MOG antibody titers stained white matter myelin in rat brain and enhanced demyelination and axonal damage when transferred to autoimmune encephalomyelitis animals. Overall these findings suggest a pathogenic antibody response to native MOG in a subgroup of MS patients."],["dc.identifier.doi","10.1073/pnas.0607242103"],["dc.identifier.isi","000242884200034"],["dc.identifier.pmid","17142321"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","179"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bittner, Alwina"],["dc.contributor.author","Schlegel, Kerstin"],["dc.contributor.author","Gronen, Felix"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Sommer, Norbert"],["dc.date.accessioned","2018-11-07T09:11:30Z"],["dc.date.available","2018-11-07T09:11:30Z"],["dc.date.issued","2006"],["dc.description.abstract","Substance P (SP) is an excitatory neurotransmitter in the central and peripheral nervous system. Most of its physiological functions are mediated through binding to the neurokinin-1 receptor (NK-1R). Recently, proinflammatory properties of SP have been described. In this study we utilized T cell transfer experimental autoimmune encephalomyelitis (EAE) to investigate the role of SP in CNS autoimmune disease. Treatment with the NK-1R antagonist CP-96,345 dramatically reduced clinical and histological signs of EAE if administered before disease onset. The protective effect of CP96,345 treatment was related to a reduced expression of the adhesion molecules ICAM-1 and VCAM-1 on CNS endothelia. The cellular composition or activation status of splenocytes was not affected by CP-96,345 administration, while the secretion of proinflammatory Thl cytokines was reduced in treated animals. Th2 cytokines remained largely unaffected by NK-1 receptor antagonist treatment. In summary, our findings suggest that the protective effect of CP96,345 treatment is mediated by stabilization of the blood-brain barrier and suppression of Thl immunity. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2006.06.026"],["dc.identifier.isi","000241821800001"],["dc.identifier.pmid","16904192"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26735"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Suppression of autoimmune encephalomyelitis by a neurokinin-1 receptor antagonist - A putative role for substance P in CNS inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","79"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Avendano-Guzman, E."],["dc.contributor.author","Theiss, R."],["dc.contributor.author","Lagumersindez-Denis, Nielsen"],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T10:08:45Z"],["dc.date.available","2018-11-07T10:08:45Z"],["dc.date.issued","2016"],["dc.description.sponsorship","Teva Pharma; Teva; Biogen; Novartis; Genzyme"],["dc.identifier.isi","000383267200129"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39531"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","London, ENGLAND"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","A new rodent model of progressive demyelination and neurodegeneration mimicking progressive MS."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","S276"],["dc.bibliographiccitation.journal","European Journal of Nuclear Medicine and Molecular Imaging"],["dc.bibliographiccitation.lastpage","S277"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Lapa, Constantin"],["dc.contributor.author","Buck, D."],["dc.contributor.author","Foerschler, Annette"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Wester, H."],["dc.contributor.author","Korn, Thomas"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Jacobi, Heike"],["dc.contributor.author","Zimmer, C."],["dc.contributor.author","Schwaiger, M."],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Krause, B."],["dc.date.accessioned","2018-11-07T08:38:09Z"],["dc.date.available","2018-11-07T08:38:09Z"],["dc.date.issued","2010"],["dc.identifier.isi","000283023800350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18703"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","1619-7070"],["dc.title","Molecular small animal imaging in an Experimental Autoimmune Encephalomyelitis (EAE) rat model"],["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","617"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","629"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Lam, Chiwah"],["dc.contributor.author","Kalluri, Sudhakar Reddy"],["dc.contributor.author","Saikali, Philippe"],["dc.contributor.author","Bautista, Katherine"],["dc.contributor.author","Dupree, Cecily"],["dc.contributor.author","Glogowska, Magdalena"],["dc.contributor.author","Case, David"],["dc.contributor.author","Antel, Jack P."],["dc.contributor.author","Owens, Gregory P."],["dc.contributor.author","Gilden, Donald H."],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T11:22:20Z"],["dc.date.available","2018-11-07T11:22:20Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: The serum of most neuromyelitis optica (NMO) patients contains autoantibodies (NMO-IgGs) directed against the aquaporin-4 (AQP4) water channel located on astrocyte foot processes in the perivessel and subpial areas of the brain. Our objectives were to determine the source of central nervous system (CNS) NMO-IgGs and their role in disease pathogenesis. Methods: Fluorescence-activated cell sorting and single-cell reverse transcriptase polymerase chain reaction were used to identify overrepresented plasma cell immunoglobulin (Ig) sequences in the cerebrospinal fluid (CSF) of an NMO patient after a first clinical attack. Monoclonal recombinant antibodies (rAbs) were generated from the paired heavy and light chain sequences and tested for target specificity and Fc effector function. The effect of CSF rAbs on CNS immunopathology was investigated by delivering single rAbs to rats with experimental autoimmune encephalomyelitis (EAE). Results: Repertoire analysis revealed a dynamic, clonally expanded plasma cell population with features of an antigen-targeted response. Using multiple independent assays, 6 of 11 rAbs generated from CSF plasma cell clones specifically bound to AQP4. AQP4-specific rAbs recognized conformational epitopes and mediated both AQP4-directed antibody-dependent cellular cytotoxicity and complement-mediated lysis. When administered to rats with EAE, an AQP4-specific NMO CSF rAb induced NMO immunopathology: perivascular astrocyte depletion, myelinolysls, and complement and Ig deposition. Interpretation: Molecular characterization of the CSF plasma cell repertoire in an early NMO patient demonstrates that AQP4-specfic Ig is synthesized intrathecally at disease onset and directly contributes to CNS pathology. AQP4 is now the first confirmed antigenic target in human demyelinating disease."],["dc.identifier.doi","10.1002/ana.21802"],["dc.identifier.isi","000272314500010"],["dc.identifier.pmid","19938104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55976"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","Intrathecal Pathogenic Anti-Aquaporin-4 Antibodies in Early Neuromyelitis Optica"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]