Weber, Martin S.

[["dc.bibliographiccitation.firstpage","e698"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology - Neuroimmunology Neuroinflammation"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Häusler, Darius"],["dc.contributor.author","Hajiyeva, Zivar"],["dc.contributor.author","Traub, Jan W."],["dc.contributor.author","Zamvil, Scott S."],["dc.contributor.author","Lalive, Patrice H."],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-04-14T08:26:30Z"],["dc.date.available","2021-04-14T08:26:30Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1212/NXI.0000000000000698"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81971"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2332-7812"],["dc.title","Glatiramer acetate immune modulates B-cell antigen presentation in treatment of MS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Kinzel, Silke"],["dc.contributor.author","Lehmann-Horn, Klaus"],["dc.contributor.author","Zamvil, Scott S."],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Bernard, Claude C."],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T09:33:33Z"],["dc.date.available","2018-11-07T09:33:33Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.026"],["dc.identifier.isi","000345192100019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31990"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Myelin-specific antibodies trigger spontaneous CNS autoimmune disease in the absence of myelin-specific B cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","9773"],["dc.bibliographiccitation.issue","39"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","9778"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Häusler, Darius"],["dc.contributor.author","Häusser-Kinzel, Silke"],["dc.contributor.author","Feldmann, Linda"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Lepennetier, Gildas"],["dc.contributor.author","Bernard, Claude C. A."],["dc.contributor.author","Zamvil, Scott S."],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Lehmann-Horn, Klaus"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-06-01T10:51:05Z"],["dc.date.available","2021-06-01T10:51:05Z"],["dc.date.issued","2018"],["dc.description.abstract","The anti-CD20 antibody ocrelizumab, approved for treatment of multiple sclerosis, leads to rapid elimination of B cells from the blood. The extent of B cell depletion and kinetics of their recovery in different immune compartments is largely unknown. Here, we studied how anti-CD20 treatment influences B cells in bone marrow, blood, lymph nodes, and spleen in models of experimental autoimmune encephalomyelitis (EAE). Anti-CD20 reduced mature B cells in all compartments examined, although a subpopulation of antigen-experienced B cells persisted in splenic follicles. Upon treatment cessation, CD20 + B cells simultaneously repopulated in bone marrow and spleen before their reappearance in blood. In EAE induced by native myelin oligodendrocyte glycoprotein (MOG), a model in which B cells are activated, B cell recovery was characterized by expansion of mature, differentiated cells containing a high frequency of myelin-reactive B cells with restricted B cell receptor gene diversity. Those B cells served as efficient antigen-presenting cells (APCs) for activation of myelin-specific T cells. In MOG peptide-induced EAE, a purely T cell-mediated model that does not require B cells, in contrast, reconstituting B cells exhibited a naive phenotype without efficient APC capacity. Our results demonstrate that distinct subpopulations of B cells differ in their sensitivity to anti-CD20 treatment and suggest that differentiated B cells persisting in secondary lymphoid organs contribute to the recovering B cell pool."],["dc.identifier.doi","10.1073/pnas.1810470115"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86889"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","Functional characterization of reappearing B cells after anti-CD20 treatment of CNS autoimmune disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2078"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","2088"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Hertzenberg, Deetje"],["dc.contributor.author","Lehmann-Horn, Klaus"],["dc.contributor.author","Kinzel, Silke"],["dc.contributor.author","Husterer, Veronika"],["dc.contributor.author","Cravens, Petra D."],["dc.contributor.author","Kieseier, Bernd C."],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Zamvil, Scott S."],["dc.contributor.author","Stueve, Olaf"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T09:21:31Z"],["dc.date.available","2018-11-07T09:21:31Z"],["dc.date.issued","2013"],["dc.description.abstract","MS is an inflammatory CNS disorder, which typically occurs in early adulthood and rarely in children. Here we tested whether functional maturation of innate immune cells may determine susceptibility to CNS autoimmune disease in EAE. Two-week-old mice were resistant to active EAE, which causes fulminant paralysis in adult mice; this resistance was associated with an impaired development of Th1 and Th17 cells. Resistant, young mice had higher frequencies of myeloid-derived suppressor cells and plasma-cytoid DCs. Furthermore, myeloid APCs and B cells from young mice expressed lower levels of MHC class II and CD40, produced decreased amounts of proinflammatory cytokines, and released enhanced levels of anti-inflammatory IL-10. When used as APCs, splenocytes from 2-week-old mice failed to differentiate naive T cells into Th1 and Th17 cells irrespective of the T-cell donor's age, and promoted development of Treg cells and Th2 cells instead. Adoptive transfer of adult APCs restored the ability of 2-week-old mice to generate encephalitogenic T cells and develop EAE. Collectively, these findings indicate that the innate immune compartment functionally matures during development, which may be a prerequisite for development of T-cell-mediated CNS autoimmune disease."],["dc.identifier.doi","10.1002/eji.201343338"],["dc.identifier.isi","000328839700012"],["dc.identifier.pmid","23637087"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29126"],["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","Developmental maturation of innate immune cell function correlates with susceptibility to central nervous system autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1315"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","JAMA Neurology"],["dc.bibliographiccitation.lastpage","1324"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Lund, Brett T."],["dc.contributor.author","Oreja-Guevara, Celia"],["dc.contributor.author","Prat, Alexandre"],["dc.contributor.author","Spencer, Collin M."],["dc.contributor.author","Steinman, Lawrence"],["dc.contributor.author","Tintore, Mar"],["dc.contributor.author","Vollmer, Timothy L."],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Weiner, Leslie P."],["dc.contributor.author","Ziemssen, Tjalf"],["dc.contributor.author","Zamvil, Scott S."],["dc.date.accessioned","2018-11-07T09:18:49Z"],["dc.date.available","2018-11-07T09:18:49Z"],["dc.date.issued","2013"],["dc.description.abstract","Several innovative disease-modifying treatments (DMTs) for relapsing-remitting multiple sclerosis have been licensed recently or are in late-stage development. The molecular targets of several of these DMTs are well defined. All affect at least 1 of 4 properties, namely (1) trafficking, (2) survival, (3) function, or (4) proliferation. In contrast to beta-interferons and glatiramer acetate, the first-generation DMTs, several newer therapies are imbued with safety issues, which may be attributed to their structure or metabolism. In addition to efficacy, understanding the relationship between the mechanism of action of the DMTs and their safety profile is pertinent for decision making and patient care. In this article, we focus primarily on the safety of DMTs in the context of understanding their pharmacological characteristics, including molecular targets, mechanism of action, chemical structure, and metabolism. While understanding mechanisms underlying DMT toxicities is incomplete, it is important to further develop this knowledge to minimize risk to patients and to ensure future therapies have the most advantageous benefit-risk profiles. Recognizing the individual classes of DMTs described here may be valuable when considering use of such agents sequentially or possibly in combination."],["dc.description.sponsorship","Teva Pharmaceuticals Inc."],["dc.identifier.doi","10.1001/jamaneurol.2013.3510"],["dc.identifier.isi","000330114400017"],["dc.identifier.pmid","23921521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28487"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","2168-6157"],["dc.relation.issn","2168-6149"],["dc.title","Therapeutic Decisions in Multiple Sclerosis Moving Beyond Efficacy"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]