Weber, Martin S.

[["dc.bibliographiccitation.firstpage","1019"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","CNS Drugs"],["dc.bibliographiccitation.lastpage","1030"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Geladaris, Anastasia"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2022-11-01T10:17:42Z"],["dc.date.available","2022-11-01T10:17:42Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s40263-022-00951-z"],["dc.identifier.pii","951"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116880"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-605"],["dc.relation.eissn","1179-1934"],["dc.relation.issn","1172-7047"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Bruton’s Tyrosine Kinase Inhibitors in Multiple Sclerosis: Pioneering the Path Towards Treatment of Progression?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","25690"],["dc.bibliographiccitation.issue","41"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","25699"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Nissimov, Nitzan"],["dc.contributor.author","Hajiyeva, Zivar"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Grondey, Katja"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Häusser-Kinzel, Silke"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-04-14T08:31:41Z"],["dc.date.available","2021-04-14T08:31:41Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1073/pnas.2012249117"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83682"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","B cells reappear less mature and more activated after their anti-CD20–mediated depletion in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e10"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain: A Journal of Neurology"],["dc.bibliographiccitation.lastpage","e10"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Häusler, Darius"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Peelen, Evelyn"],["dc.contributor.author","Bertsch, Thomas"],["dc.contributor.author","Weber, Matthias"],["dc.contributor.author","Heilmann, Marcus"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Larochelle, Catherine"],["dc.contributor.author","Zamvil, Scott S"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Weber, Martin S"],["dc.date.accessioned","2021-04-14T08:27:32Z"],["dc.date.available","2021-04-14T08:27:32Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1093/brain/awz389"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82322"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","Reply: Neither human nor mouse is hypercalcaemic with 250 nmol/l 25-hydroxyvitamin D"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","535"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","548"],["dc.bibliographiccitation.volume","140"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Pretzsch, Roxanne"],["dc.contributor.author","Häusler, Darius"],["dc.contributor.author","Haselmayer, Philipp"],["dc.contributor.author","Grenningloh, Roland"],["dc.contributor.author","Boschert, Ursula"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-04-14T08:24:46Z"],["dc.date.available","2021-04-14T08:24:46Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00401-020-02204-z"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81418"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Inhibition of Bruton’s tyrosine kinase interferes with pathogenic B-cell development in inflammatory CNS demyelinating disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","1143"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Expert Opinion on Investigational Drugs"],["dc.bibliographiccitation.lastpage","1150"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-04-14T08:24:18Z"],["dc.date.available","2021-04-14T08:24:18Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1080/13543784.2020.1807934"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81241"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1744-7658"],["dc.relation.issn","1354-3784"],["dc.title","Inhibition of Bruton´s tyrosine kinase as a novel therapeutic approach in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","638"],["dc.bibliographiccitation.journal","Science Translational Medicine"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Ochs, Jasmin"],["dc.contributor.author","Nissimov, Nitzan"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Freier, Marie"],["dc.contributor.author","Grondey, Katja"],["dc.contributor.author","Koch, Julian"],["dc.contributor.author","Klein, Matthias"],["dc.contributor.author","Feldmann, Linda"],["dc.contributor.author","Gudd, Cathrin"],["dc.contributor.author","Bopp, Tobias"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2022-04-01T10:01:55Z"],["dc.date.available","2022-04-01T10:01:55Z"],["dc.date.issued","2022"],["dc.description.abstract","The origin and function of CD20 + T cells are poorly understood. Here, we characterized CD20 + T cells in mice and humans and investigated how they are affected by anti-CD20 antibody treatment. We report that murine CD20 + T cells are unable to endogenously express the B cell lineage marker CD20; the development of CD20 + T cells in rodents requires the presence of CD20-expressing B cells. Our results demonstrated that both murine and human T cells acquire CD20 from B cells via trogocytosis while being activated by an antigen-presenting B cell. In patients with multiple sclerosis (MS) and mice with experimental autoimmune encephalomyelitis (EAE), expression of CD20 on T cells is associated with an up-regulation of activation markers, proinflammatory cytokines, and adhesion molecules, suggesting high pathogenic potential. Supporting this hypothesis, CD20 + T cells expand during active EAE in rodents; furthermore, adoptive transfer of CD20 + T cells into EAE-diseased mice worsened histological and clinical severity. Of direct therapeutic relevance, we demonstrate that the exclusive therapeutic elimination of CD20 + T cells effectively ameliorates EAE, independent of B cells. The results support the hypothesis that CD20 + T cells arise upon B cell–T cell interaction and that depletion of CD20 + T cells might contribute to the success of anti-CD20 antibody therapies in MS and other inflammatory disorders."],["dc.identifier.doi","10.1126/scitranslmed.abi4632"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105780"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1946-6242"],["dc.relation.issn","1946-6234"],["dc.title","Proinflammatory CD20 + T cells contribute to CNS-directed autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]