Flügel, Alexander

[["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:11:32Z"],["dc.date.available","2018-11-07T09:11:32Z"],["dc.date.issued","2012"],["dc.identifier.isi","000303204801256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26744"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","64th Annual Meeting of the American-Academy-of-Neurology (AAN)"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0028-3878"],["dc.title","Analysis of Laquinimod Efficiency during Experimental Autoimmune Encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S340"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","S341"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T08:51:28Z"],["dc.date.available","2018-11-07T08:51:28Z"],["dc.date.issued","2011"],["dc.identifier.isi","000209137301134"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21940"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Analysis of laquinimod efficiency during experimental autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","202"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Linker, Ralf"],["dc.contributor.author","Lee, De-hyung"],["dc.contributor.author","Reichardt, Holger"],["dc.contributor.author","Bommhardt, Ursula"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:33:36Z"],["dc.date.available","2018-11-07T09:33:36Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.544"],["dc.identifier.isi","000345192100533"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32000"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","12th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.title","Critical role of thymocyte-derived brain-derived neurotrophic factor in T cell maturation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8486"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","22"],["dc.contributor.affiliation","Hülskötter, Kirsten; \t\t \r\n\t\t Department of Pathology, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany, kirsten.huelskoetter@tiho-hannover.de\t\t \r\n\t\t Center for Systems Neuroscience, 30559 Hannover, Germany, kirsten.huelskoetter@tiho-hannover.de"],["dc.contributor.affiliation","Lühder, Fred; \t\t \r\n\t\t Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany, fred.luehder@med.uni-goettingen.de"],["dc.contributor.affiliation","Flügel, Alexander; \t\t \r\n\t\t Center for Systems Neuroscience, 30559 Hannover, Germany, fluegel@med.uni-goettingen.de\t\t \r\n\t\t Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany, fluegel@med.uni-goettingen.de"],["dc.contributor.affiliation","Herder, Vanessa; \t\t \r\n\t\t Department of Pathology, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany, vanessa.herder@tiho-hannover.de\t\t \r\n\t\t Center for Systems Neuroscience, 30559 Hannover, Germany, vanessa.herder@tiho-hannover.de"],["dc.contributor.affiliation","Baumgärtner, Wolfgang; \t\t \r\n\t\t Department of Pathology, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany, Wolfgang.baumgaertner@tiho-hannover.de\t\t \r\n\t\t Center for Systems Neuroscience, 30559 Hannover, Germany, Wolfgang.baumgaertner@tiho-hannover.de"],["dc.contributor.author","Hülskötter, Kirsten"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Herder, Vanessa"],["dc.contributor.author","Baumgärtner, Wolfgang"],["dc.date.accessioned","2021-10-01T09:58:26Z"],["dc.date.available","2021-10-01T09:58:26Z"],["dc.date.issued","2021"],["dc.date.updated","2022-09-04T01:37:29Z"],["dc.description.abstract","Tamoxifen is frequently used in murine knockout systems with CreER/LoxP. Besides possible neuroprotective effects, tamoxifen is described as having a negative impact on adult neurogenesis. The present study investigated the effect of a high-dose tamoxifen application on Theiler’s murine encephalomyelitis virus (TMEV)-induced hippocampal damage. Two weeks after TMEV infection, 42% of the untreated TMEV-infected mice were affected by marked inflammation with neuronal loss, whereas 58% exhibited minor inflammation without neuronal loss. Irrespective of the presence of neuronal loss, untreated mice lacked TMEV antigen expression within the hippocampus at 14 days post-infection (dpi). Interestingly, tamoxifen application 0, 2 and 4, or 5, 7 and 9 dpi decelerated virus elimination and markedly increased neuronal loss to 94%, associated with increased reactive astrogliosis at 14 dpi. T cell infiltration, microgliosis and expression of water channels were similar within the inflammatory lesions, regardless of tamoxifen application. Applied at 0, 2 and 4 dpi, tamoxifen had a negative impact on the number of doublecortin (DCX)-positive cells within the dentate gyrus (DG) at 14 dpi, without a long-lasting effect on neuronal loss at 147 dpi. Thus, tamoxifen application during a TMEV infection is associated with transiently increased neuronal loss in the hippocampus, increased reactive astrogliosis and decreased neurogenesis in the DG."],["dc.description.abstract","Tamoxifen is frequently used in murine knockout systems with CreER/LoxP. Besides possible neuroprotective effects, tamoxifen is described as having a negative impact on adult neurogenesis. The present study investigated the effect of a high-dose tamoxifen application on Theiler’s murine encephalomyelitis virus (TMEV)-induced hippocampal damage. Two weeks after TMEV infection, 42% of the untreated TMEV-infected mice were affected by marked inflammation with neuronal loss, whereas 58% exhibited minor inflammation without neuronal loss. Irrespective of the presence of neuronal loss, untreated mice lacked TMEV antigen expression within the hippocampus at 14 days post-infection (dpi). Interestingly, tamoxifen application 0, 2 and 4, or 5, 7 and 9 dpi decelerated virus elimination and markedly increased neuronal loss to 94%, associated with increased reactive astrogliosis at 14 dpi. T cell infiltration, microgliosis and expression of water channels were similar within the inflammatory lesions, regardless of tamoxifen application. Applied at 0, 2 and 4 dpi, tamoxifen had a negative impact on the number of doublecortin (DCX)-positive cells within the dentate gyrus (DG) at 14 dpi, without a long-lasting effect on neuronal loss at 147 dpi. Thus, tamoxifen application during a TMEV infection is associated with transiently increased neuronal loss in the hippocampus, increased reactive astrogliosis and decreased neurogenesis in the DG."],["dc.identifier.doi","10.3390/ijms22168486"],["dc.identifier.pii","ijms22168486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90061"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Tamoxifen Application Is Associated with Transiently Increased Loss of Hippocampal Neurons following Virus Infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","95"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Archivum Immunologiae et Therapiae Experimentalis"],["dc.bibliographiccitation.lastpage","105"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2018-11-07T09:26:46Z"],["dc.date.available","2018-11-07T09:26:46Z"],["dc.date.issued","2013"],["dc.description.abstract","The concept of neuroprotective autoimmunity implies that immune cells, especially autoantigen-specific T cells, infiltrate the central nervous system (CNS) after injury and contribute to neuroregeneration and repair by secreting soluble factors. Amongst others, neurotrophic factors and neurotrophins such as brain-derived neurotropic factor (BDNF) are considered to play an important role in this process. New data raise the possibility that this concept could also be extended to neuroinflammatory diseases such as multiple sclerosis (MS) where autoantigen-specific T cells infiltrate the CNS, causing axonal/neuronal damage on the one hand, but also providing neuroprotective support on the other hand. In this review, we summarize the current knowledge on BDNF levels analyzed in MS patients in different compartments and its correlation with clinical parameters. Furthermore, new approaches in experimental animal models are discussed that attempt to decipher the functional relevance of BDNF in autoimmune demyelination."],["dc.identifier.doi","10.1007/s00005-012-0211-0"],["dc.identifier.isi","000316199800001"],["dc.identifier.pmid","23283517"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30378"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Basel"],["dc.relation.issn","0004-069X"],["dc.title","Brain-Derived Neurotrophic Factor in Neuroimmunology: Lessons Learned from Multiple Sclerosis Patients and Experimental Autoimmune Encephalomyelitis Models"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S3"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","S11"],["dc.bibliographiccitation.volume","311"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Schlaeger, Christian"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Odoardi, Francesca"],["dc.date.accessioned","2018-11-07T08:49:03Z"],["dc.date.available","2018-11-07T08:49:03Z"],["dc.date.issued","2011"],["dc.description.abstract","Current concepts attribute an early and central role for auto-aggressive, myelin-specific T-lymphocytes in the pathogenesis of multiple sclerosis. This view emerged from immunological and pathological findings in experimental autoimmune encephalitis, an animal model characterised by pathological lesions closely resembling the ones found in multiple sclerosis. Furthermore, therapeutic strategies targeting the functions of these encephalitogenic T cells which attenuate their pathogenicity such as glatiramer acetate or anti-VLA4 antibody treatments represent proven approaches in multiple sclerosis. Nonetheless, all therapies evaluated to date either insufficiently dampen down inflammation or completely block immune processes. For this reason, there is a need to identify new therapeutic targets. We have employed live intravital two-photon microscopy to learn more about the behaviour of T cells during the preclinical phase of EAE, when T cells acquire the properties required to invade their target organ. Furthermore, we were able to identify an unexpected locomotive behaviour of T cells at the blood-brain barrier, which occurs immediately before diapedesis and the induction of paralytic disease. Such studies might open new avenues for the treatment of CNS autoimmune diseases. Multiple sclerosis is considered to be an autoimmune disease in which self-reactive T cells enter the central nervous system (CNS) and create an inflammatory milieu that destroys myelin and neurons. Immunomodulatory strategies for the treatment of multiple sclerosis target this process by attempting to inactivate these auto-aggressive T cells. However, so far, these strategies have failed to extinguish disease activity completely. For this reason, there is a need to understand in more detail the mechanisms by which T cells become encephalitogenic, how they enter the nervous system, and what the signals are that guide them along this path. If these processes could be better understood, it may be possible to design more effective and specific therapies for multiple sclerosis. This article will give a brief overview about our recent findings obtained using intravital imaging of autoaggressive effector T cells in an experimental model of multiple sclerosis. This new technological approach might help to fill some gaps in the understanding of autoimmune pathogenesis of multiple sclerosis. (C) 2011 Elsevier B.V. All rights reserved."],["dc.identifier.isi","000299446300002"],["dc.identifier.pmid","22206764"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21360"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0022-510X"],["dc.title","Autoimmune disease in the brain - how to spot the culprits and how to keep them in check"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","247"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","258"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Geyer, Eva"],["dc.contributor.author","Flach, Anne-Christine"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Luehder, Fred"],["dc.date.accessioned","2018-11-07T09:13:35Z"],["dc.date.available","2018-11-07T09:13:35Z"],["dc.date.issued","2012"],["dc.description.abstract","Brain-derived neurotrophic factor (BDNF) is involved in neuronal and glial development and survival. While neurons and astrocytes are its main cellular source in the central nervous system (CNS), bioactive BDNF is also expressed in immune cells and in lesions of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Previous data revealed that BDNF exerts neuroprotective effects in myelin oligodendrocyte glycoprotein-induced EAE. Using a conditional knock-out model with inducible deletion of BDNF, we here show that clinical symptoms and structural damage are increased when BDNF is absent during the initiation phase of clinical EAE. In contrast, deletion of BDNF later in the disease course of EAE did not result in significant changes, either in the disease course or in axonal integrity. Bone marrow chimeras revealed that the deletion of BDNF in the CNS alone, with no deletion of BDNF in the infiltrating immune cells, was sufficient for the observed effects. Finally, the therapeutic effect of glatiramer acetate, a well-characterized disease-modifying drug with the potential to modulate BDNF expression, was partially reversed in mice in which BDNF was deleted shortly before the onset of disease. In summary, our data argue for an early window of therapeutic opportunity where modulation of BDNF may exert neuroprotective effects in experimental autoimmune demyelination."],["dc.identifier.doi","10.1007/s00401-011-0890-3"],["dc.identifier.isi","000301855900008"],["dc.identifier.pmid","22009304"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27216"],["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","Central nervous system rather than immune cell-derived BDNF mediates axonal protective effects early in autoimmune demyelination"],["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","1326"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","1338"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Flach, Anne-Christine"],["dc.contributor.author","Litke, Tanja"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Lingner, Thomas"],["dc.contributor.author","Bommhardt, Ursula"],["dc.contributor.author","Sendtner, Michael"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Luehder, Fred"],["dc.date.accessioned","2018-11-07T09:57:51Z"],["dc.date.available","2018-11-07T09:57:51Z"],["dc.date.issued","2015"],["dc.description.abstract","Brain-derived neurotrophic factor (BDNF) promotes neuronal survival, regeneration, and plasticity. Emerging evidence also indicates an essential role for BDNF outside the nervous system, for instance in immune cells. We therefore investigated the impact of BDNF on Tcells using BDNF knockout (KO) mice and conditional KO mice lacking BDNF specifically in this lymphoid subset. In both settings, we observed diminished T-cell cellularity in peripheral lymphoid organs and an increase in CD4(+)CD44(+) memory Tcells. Analysis of thymocyte development revealed diminished total thymocyte numbers, accompanied by a significant increase in CD4/CD8 double-negative (DN) thymocytes due to a partial block in the transition from the DN3 to the DN4 stage. This was neither due to increased thymocyte apoptosis nor defects in the expression of the TCR- chain or the pre-TCR. In contrast, pERK but not pAKT levels were diminished in DN3 BDNF-deficient thymocytes. BDNF deficiency in Tcells did not result in gross deficits in peripheral acute immune responses nor in changes of the homeostatic proliferation of peripheral Tcells. Taken together, our data reveal a critical autocrine and/or paracrine role of T-cell-derived BDNF in thymocyte maturation involving ERK-mediated TCR signaling pathways."],["dc.identifier.doi","10.1002/eji.201444985"],["dc.identifier.isi","000354182300006"],["dc.identifier.pmid","25627579"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37248"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.title","Thymocyte-derived BDNF influences T-cell maturation at the DN3/DN4 transition stage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Brain Pathology"],["dc.contributor.author","Hülskötter, Kirsten"],["dc.contributor.author","Jin, Wen"],["dc.contributor.author","Allnoch, Lisa"],["dc.contributor.author","Hansmann, Florian"],["dc.contributor.author","Schmidtke, Daniel"],["dc.contributor.author","Rohn, Karl"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Baumgärtner, Wolfgang"],["dc.contributor.author","Herder, Vanessa"],["dc.date.accessioned","2021-08-12T07:45:21Z"],["dc.date.available","2021-08-12T07:45:21Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1111/bpa.12994"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88436"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","1750-3639"],["dc.relation.issn","1015-6305"],["dc.title","Double‐edged effects of tamoxifen‐in‐oil‐gavage on an infectious murine model for multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3323"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","3328"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Flach, Anne-Christine"],["dc.contributor.author","Litke, Tanja"],["dc.contributor.author","Strauss, Judith"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Gomez, Cesar Cordero"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Saiz, Albert"],["dc.contributor.author","Fehling, Hans-Joerg"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T10:16:44Z"],["dc.date.available","2018-11-07T10:16:44Z"],["dc.date.issued","2016"],["dc.description.abstract","Multiple sclerosis (MS) is caused by T cells that are reactive for brain antigens. In experimental autoimmune encephalomyelitis, the animal model for MS, myelin-reactive T cells initiate the autoimmune process when entering the nervous tissue and become reactivated upon local encounter of their cognate CNS antigen. Thereby, the strength of the T-cellular reactivation process within the CNS tissue is crucial for the manifestation and the severity of the clinical disease. Recently, B cells were found to participate in the pathogenesis of CNS autoimmunity, with several diverse underlying mechanisms being under discussion. We here report that B cells play an important role in promoting the initiation process of CNS autoimmunity. Myelin-specific antibodies produced by autoreactive B cells after activation in the periphery diffused into the CNS together with the first invading pathogenic T cells. The antibodies accumulated in resident antigen-presenting phagocytes and significantly enhanced the activation of the incoming effector T cells. The ensuing strong blood-brain barrier disruption and immune cell recruitment resulted in rapid manifestation of clinical disease. Therefore, myelin oligodendrocyte glycoprotein (MOG)-specific autoantibodies can initiate disease bouts by cooperating with the autoreactive T cells in helping them to recognize their autoantigen and become efficiently reactivated within the immune-deprived nervous tissue."],["dc.identifier.doi","10.1073/pnas.1519608113"],["dc.identifier.isi","000372488200061"],["dc.identifier.pmid","26957602"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41093"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Autoantibody-boosted T-cell reactivation in the target organ triggers manifestation of autoimmune CNS disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]