Brück, Wolfgang

[["dc.bibliographiccitation.firstpage","1590"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1593"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:39:53Z"],["dc.date.available","2018-11-07T08:39:53Z"],["dc.date.issued","2010"],["dc.description.abstract","The following review summarizes the progress in multiple sclerosis research published in the Journal of Neurology in 2009."],["dc.identifier.doi","10.1007/s00415-010-5689-y"],["dc.identifier.isi","000281250100031"],["dc.identifier.pmid","20689961"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5157"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19106"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Advances in multiple sclerosis research in 2009"],["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","235"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Radue, Ernst-Wilhelm"],["dc.contributor.author","Oterino, Agustin"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Schippling, Sven"],["dc.contributor.author","Kuhle, Jens"],["dc.contributor.author","Sahraian, Mohammad Ali"],["dc.contributor.author","Gray, Francoise"],["dc.contributor.author","Jakl, Veronika"],["dc.contributor.author","Haeusler, Darius"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:13:35Z"],["dc.date.available","2018-11-07T09:13:35Z"],["dc.date.issued","2012"],["dc.description.abstract","Natalizumab is an approved medication for highly active multiple sclerosis (MS). Progressive multifocal leukoencephalopathy (PML) may occur as a severe side effect of this drug. Here, we describe pathological and radiological characteristics of immune reconstitution inflammatory syndrome (IRIS), which occurs in natalizumab-associated PML after the cessation of therapy, and we differentiate it from ongoing PML. Brain biopsy tissue and MRI scans from five MS patients with natalizumab-associated PML were analyzed and their histology compared with non-MS PML. Histology showed an extensive CD8-dominated T cell infiltrate and numerous macrophages within lesions, and in nondemyelinated white and grey matter, in four out of five cases. Few or no virally infected cells were found. This was indicative of IRIS as known from HIV patients with PML. Outstandingly high numbers of plasma cells were present as compared to non-MS PML and typical MS lesions. MRI was compatible with IRIS, revealing enlarging lesions with a band-like or speckled contrast enhancement either at the lesion edge or within lesions. Only the fifth patient showed typical PML pathology, with low inflammation and high numbers of virally infected cells. This patient showed a similar interval between drug withdrawal and biopsy (3.5 months) to the rest of the cohort (range 2.5-4 months). MRI could not differentiate between PML-associated IRIS and ongoing PML. We describe in detail the histopathology of IRIS in natalizumab-associated PML. PML-IRIS, ongoing PML infection, and MS exacerbation may be impossible to discern clinically alone. MRI may provide some clues for distinguishing different pathologies that can be differentiated histologically. In our individual cases, biopsy helped to clarify diagnoses in natalizumab-associated PML."],["dc.identifier.doi","10.1007/s00401-011-0900-5"],["dc.identifier.isi","000301855900007"],["dc.identifier.pmid","22057786"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7121"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27215"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Pathology of immune reconstitution inflammatory syndrome in multiple sclerosis with natalizumab-associated progressive multifocal leukoencephalopathy"],["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","81"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Rieckmann, Peter"],["dc.contributor.author","Kallmann, Boris-Alexander"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2019-07-09T11:42:51Z"],["dc.date.available","2019-07-09T11:42:51Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1186/s40478-016-0352-1"],["dc.identifier.pmid","27503238"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58763"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Disseminated necrotizing leukoencephalopathy eight months after alemtuzumab treatment for multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13275"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Romanelli, Elisa"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Mezydlo, Aleksandra"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Nikic, Ivana"],["dc.contributor.author","Potz, Stephanie"],["dc.contributor.author","Meinl, Edgar"],["dc.contributor.author","Matznick, Florian E. H."],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Ghanem, Alexander"],["dc.contributor.author","Conzelmann, Karl-Klaus"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Routh, Matthew"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Bishop, Derron"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.date.accessioned","2018-11-07T10:05:43Z"],["dc.date.available","2018-11-07T10:05:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Oligodendrocyte damage is a central event in the pathogenesis of the common neuro-inflammatory condition, multiple sclerosis (MS). Where and how oligodendrocyte damage is initiated in MS is not completely understood. Here, we use a combination of light and electron microscopy techniques to provide a dynamic and highly resolved view of oligodendrocyte damage in neuroinflammatory lesions. We show that both in MS and in its animal model structural damage is initiated at the myelin sheaths and only later spreads to the oligodendrocyte cell body. Early myelin damage itself is characterized by the formation of local myelin out-foldings-'myelinosomes'-, which are surrounded by phagocyte processes and promoted in their formation by anti-myelin antibodies and complement. The presence of myelinosomes in actively demyelinating MS lesions suggests that oligodendrocyte damage follows a similar pattern in the human disease, where targeting demyelination by therapeutic interventions remains a major open challenge."],["dc.identifier.doi","10.1038/ncomms13275"],["dc.identifier.isi","000387837900001"],["dc.identifier.pmid","27848954"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13963"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38953"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["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","Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model"],["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","e33"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology® neuroimmunology & neuroinflammation"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Thomas, Katja"],["dc.contributor.author","Dietze, Kristin"],["dc.contributor.author","Wehner, Rebekka"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Schultheiß, Thorsten"],["dc.contributor.author","Günther, Claudia"],["dc.contributor.author","Schäkel, Knut"],["dc.contributor.author","Reichmann, Heinz"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Schmitz, Marc"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.date.accessioned","2015-10-20T13:57:53Z"],["dc.date.accessioned","2021-10-27T13:20:20Z"],["dc.date.available","2015-10-20T13:57:53Z"],["dc.date.available","2021-10-27T13:20:20Z"],["dc.date.issued","2014-10-01"],["dc.description.abstract","OBJECTIVE: To examine the potential role of 6-sulfo LacNAc(+) (slan) dendritic cells (DCs) displaying pronounced proinflammatory properties in the pathogenesis of multiple sclerosis (MS). METHODS: We determined the presence of slanDCs in demyelinated brain lesions and CSF samples of patients with MS. In addition, we explored the impact of methylprednisolone, interferon-β, glatiramer acetate, or natalizumab on the frequency of blood-circulating slanDCs in patients with MS. We also evaluated whether interferon-β modulates important proinflammatory capabilities of slanDCs. RESULTS: SlanDCs accumulate in highly inflammatory brain lesions and are present in the majority of CSF samples of patients with MS. Short-term methylprednisolone administration reduces the percentage of slanDCs in blood of patients with MS and the proportion of tumor necrosis factor-α- or CD150-expressing slanDCs. Long-term interferon-β treatment decreases the percentage of blood-circulating slanDCs in contrast to glatiramer acetate or natalizumab. Furthermore, interferon-β inhibits the secretion of proinflammatory cytokines by slanDCs and their capacity to promote proliferation and differentiation of T cells. CONCLUSION: Accumulation of slanDCs in highly inflammatory brain lesions and their presence in CSF indicate that slanDCs may play an important role in the immunopathogenesis of MS. The reduction of blood-circulating slanDCs and the inhibition of their proinflammatory properties by methylprednisolone and interferon-β may contribute to the therapeutic efficiency of these drugs in patients with MS."],["dc.identifier.doi","10.1212/NXI.0000000000000033"],["dc.identifier.fs","611429"],["dc.identifier.pmid","25340085"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12196"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91957"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2332-7812"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Accumulation and therapeutic modulation of 6-sulfo LacNAc(+) dendritic cells in multiple sclerosis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","471"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.lastpage","482"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Lindquist, S."],["dc.contributor.author","Bodammer, N."],["dc.contributor.author","Kaufmann, J."],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Heinze, H-J"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Sailer, M."],["dc.date.accessioned","2018-11-07T11:02:56Z"],["dc.date.available","2018-11-07T11:02:56Z"],["dc.date.issued","2007"],["dc.description.abstract","Defining tools in magnetic resonance imaging (MRI) representing specific pathological processes is needed to understand the complex relationship between inflammation, myelin breakdown, axonal injury and clinical symptoms in multiple sclerosis (MS) and its variants. Here, we describe a case of histologically-defined MS, in which the radiological appearance of the lesion and clinical course support the diagnosis of Balo's concentric sclerosis. Serial magnetization transfer, diffusion tensor imaging and H-1-magnetic resonance spectroscopy, from 14 days to 13 months after biopsy, allow the contextual interpretation of specific pathological changes. In our case, acute inflammation was sensitively traced by fractional anisotropy and increased lactate in spectroscopy. In contrast, magnetization transfer ratio and the apparent diffusion coefficient monitor the sequential loss of tissue in selected rings of the lesion. The delay from the peak of symptoms in a dramatic clinical course to the maximum tissue destruction indicated through MRI suggests that compromise of axonal function may be decisive for the acute clinical situation. This is the first report comparing H-1-magnetic resonance spectroscopy, magnetization transfer and diffusion tensor imaging with histopathology in a patient with Balo's concentric sclerosis."],["dc.identifier.doi","10.1177/1352458506071329"],["dc.identifier.isi","000246845000005"],["dc.identifier.pmid","17463070"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51499"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1352-4585"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Histopathology and serial, multimodal magnetic resonance imaging in a multiple sclerosis variant"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1182"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Intensive Care Medicine"],["dc.bibliographiccitation.lastpage","1191"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Heuer, J. F."],["dc.contributor.author","Pelosi, Paolo"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Crozier, Thomas A."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Quintel, Michael"],["dc.date.accessioned","2018-11-07T08:54:47Z"],["dc.date.available","2018-11-07T08:54:47Z"],["dc.date.issued","2011"],["dc.description.abstract","To determine reciprocal and synergistic effects of acute intracranial hypertension and ARDS on neuronal and pulmonary damage and to define possible mechanisms. Twenty-eight mechanically ventilated pigs were randomized to four groups of seven each: control; acute intracranial hypertension (AICH); acute respiratory distress syndrome (ARDS); acute respiratory distress syndrome in combination with acute intracranial hypertension (ARDS + AICH). AICH was induced with an intracranial balloon catheter and the inflation volume was adjusted to keep intracranial pressure (ICP) at 30-40 cmH(2)O. ARDS was induced by oleic acid infusion. Respiratory function, hemodynamics, extravascular lung water index (ELWI), lung and brain computed tomography (CT) scans, as well as inflammatory mediators, S100B, and neuronal serum enolase (NSE) were measured over a 4-h period. Lung and brain tissue were collected and examined at the end of the experiment. In both healthy and injured lungs, AICH caused increases in NSE and TNF-alpha plasma concentrations, extravascular lung water, and lung density in CT, the extent of poorly aerated (dystelectatic) and atelectatic lung regions, and an increase in the brain tissue water content. ARDS and AICH in combination induced damage in the hippocampus and decreased density in brain CT. AICH induces lung injury and also exacerbates pre-existing damage. Increased extravascular lung water is an early marker. ARDS has a detrimental effect on the brain and acts synergistically with intracranial hypertension to cause histological hippocampal damage."],["dc.identifier.doi","10.1007/s00134-011-2232-2"],["dc.identifier.isi","000292286800020"],["dc.identifier.pmid","21544692"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7288"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22752"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0342-4642"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Acute effects of intracranial hypertension and ARDS on pulmonary and neuronal damage: a randomized experimental study in pigs"],["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","1840"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Akkermann, Dagmar"],["dc.contributor.author","Schütza, Vlad"],["dc.contributor.author","Abdelaal, Tamer A."],["dc.contributor.author","Hermes, Doris"],["dc.contributor.author","Schäffner, Erik"],["dc.contributor.author","Soto-Bernardini, M. Clara"],["dc.contributor.author","Götze, Tilmann"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Krueger, Martin"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Frydrychowicz, Clara"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Mueller, Wolf C."],["dc.contributor.author","Bechmann, Ingo"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Stassart, Ruth M."],["dc.date.accessioned","2019-07-09T11:51:38Z"],["dc.date.available","2019-07-09T11:51:38Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41467-019-09886-4"],["dc.identifier.pmid","30992451"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16160"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59979"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Publisher Correction: NRG1 type I dependent autoparacrine stimulation of Schwann cells in onion bulbs of peripheral neuropathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1762"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1764"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Goertz, Chantima"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Berlit, Peter"],["dc.date.accessioned","2018-11-07T08:38:38Z"],["dc.date.available","2018-11-07T08:38:38Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1007/s00415-010-5611-7"],["dc.identifier.isi","000282700300032"],["dc.identifier.pmid","20559846"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18807"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Primary angiitis of the CNS with pure spinal cord involvement: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","43"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","58"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Kinzel, Silke"],["dc.contributor.author","Lehmann-Horn, Klaus"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Haeusler, Darius"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Payne, Natalie L."],["dc.contributor.author","Feldmann, Linda"],["dc.contributor.author","Saiz, Albert"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Lalive, Patrice H."],["dc.contributor.author","Bernard, Claude C."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T10:12:20Z"],["dc.date.available","2018-11-07T10:12:20Z"],["dc.date.issued","2016"],["dc.description.abstract","In the pathogenesis of central nervous system (CNS) demyelinating disorders, antigen-specific B cells are implicated to act as potent antigen-presenting cells (APC), eliciting waves of inflammatory CNS infiltration. Here, we provide the first evidence that CNS-reactive antibodies (Ab) are similarly capable of initiating an encephalitogenic immune response by targeting endogenous CNS antigen to otherwise inert myeloid APC. In a transgenic mouse model, constitutive production of Ab against myelin oligodendrocyte glycoprotein (MOG) was sufficient to promote spontaneous experimental autoimmune encephalomyelitis (EAE) in the absence of B cells, when mice endogenously contained MOG-recognizing T cells. Adoptive transfer studies corroborated that anti-MOG Ab triggered activation and expansion of peripheral MOG-specific T cells in an Fc-dependent manner, subsequently causing EAE. To evaluate the underlying mechanism, anti-MOG Ab were added to a co-culture of myeloid APC and MOG-specific T cells. At otherwise undetected concentrations, anti-MOG Ab enabled Fc-mediated APC recognition of intact MOG; internalized, processed and presented MOG activated na < ve T cells to differentiate in an encephalitogenic manner. In a series of translational experiments, anti-MOG Ab from two patients with an acute flare of CNS inflammation likewise facilitated detection of human MOG. Jointly, these observations highlight Ab-mediated opsonization of endogenous CNS auto-antigen as a novel disease- and/or relapse-triggering mechanism in CNS demyelinating disorders."],["dc.identifier.doi","10.1007/s00401-016-1559-8"],["dc.identifier.isi","000378811600003"],["dc.identifier.pmid","27022743"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14069"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40217"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["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","Myelin-reactive antibodies initiate T cell-mediated CNS autoimmune disease by opsonization of endogenous antigen"],["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"]]