Stadelmann-Nessler, Christine

[["dc.bibliographiccitation.firstpage","768"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Annals of clinical and translational neurology"],["dc.bibliographiccitation.lastpage","783"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Malviya, Manish"],["dc.contributor.author","Barman, Sumanta"],["dc.contributor.author","Golombeck, Kristin S."],["dc.contributor.author","Planagumà, Jesús"],["dc.contributor.author","Mannara, Francesco"],["dc.contributor.author","Strutz-Seebohm, Nathalie"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Demir, Fatih"],["dc.contributor.author","Baksmeier, Christine"],["dc.contributor.author","Steckel, Julia"],["dc.contributor.author","Falk, Kim Kristin"],["dc.contributor.author","Gross, Catharina C."],["dc.contributor.author","Kovac, Stjepana"],["dc.contributor.author","Bönte, Kathrin"],["dc.contributor.author","Johnen, Andreas"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Martín-García, Elena"],["dc.contributor.author","Becker, Albert J."],["dc.contributor.author","Elger, Christian E."],["dc.contributor.author","Klöcker, Nikolaj"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Meuth, Sven G."],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Seebohm, Guiscard"],["dc.contributor.author","Leypoldt, Frank"],["dc.contributor.author","Maldonado, Rafael"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Dalmau, Josep"],["dc.contributor.author","Melzer, Nico"],["dc.contributor.author","Goebels, Norbert"],["dc.date.accessioned","2019-07-09T11:44:45Z"],["dc.date.available","2019-07-09T11:44:45Z"],["dc.date.issued","2017-11"],["dc.description.abstract","Objective: Autoimmune encephalitis is most frequently associated with anti-NMDAR autoantibodies. Their pathogenic relevance has been suggested by passive transfer of patients' cerebrospinal fluid (CSF) in mice in vivo. We aimed to analyze the intrathecal plasma cell repertoire, identify autoantibody-producing clones, and characterize their antibody signatures in recombinant form. Methods: Patients with recent onset typical anti-NMDAR encephalitis were subjected to flow cytometry analysis of the peripheral and intrathecal immune response before, during, and after immunotherapy. Recombinant human monoclonal antibodies (rhuMab) were cloned and expressed from matching immunoglobulin heavy- (IgH) and light-chain (IgL) amplicons of clonally expanded intrathecal plasma cells (cePc) and tested for their pathogenic relevance. Results: Intrathecal accumulation of B and plasma cells corresponded to the clinical course. The presence of cePc with hypermutated antigen receptors indicated an antigen-driven intrathecal immune response. Consistently, a single recombinant human GluN1-specific monoclonal antibody, rebuilt from intrathecal cePc, was sufficient to reproduce NMDAR epitope specificity in vitro. After intraventricular infusion in mice, it accumulated in the hippocampus, decreased synaptic NMDAR density, and caused severe reversible memory impairment, a key pathogenic feature of the human disease, in vivo. Interpretation: A CNS-specific humoral immune response is present in anti-NMDAR encephalitis specifically targeting the GluN1 subunit of the NMDAR. Using reverse genetics, we recovered the typical intrathecal antibody signature in recombinant form, and proved its pathogenic relevance by passive transfer of disease symptoms from man to mouse, providing the critical link between intrathecal immune response and the pathogenesis of anti-NMDAR encephalitis as a humorally mediated autoimmune disease."],["dc.identifier.doi","10.1002/acn3.444"],["dc.identifier.pmid","29159189"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59083"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2328-9503"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","NMDAR encephalitis: passive transfer from man to mouse by a recombinant antibody."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","698"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","704"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Schirmer, Lucas"],["dc.contributor.author","Albert, Monika"],["dc.contributor.author","Buss, Armin"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Antel, Jack P."],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2019-07-09T11:52:53Z"],["dc.date.available","2019-07-09T11:52:53Z"],["dc.date.issued","2009"],["dc.description.abstract","Research in multiple sclerosis (MS) has recently been focusing on the extent of neuroaxonal damage and its contribution to disease outcome. In the present study, we examined spinal cord tissue from 30 clinically well-characterized MS patients. MS, amyotrophic lateral sclerosis (ALS), and control spinal cord tissue were subjected to morphometric analysis and immunohistochemistry for markers of cell damage and regeneration. Data were related to disease duration and age at death. Here, we present evidence for substantial, nonprogressive neuronal loss on the cervical and lumbar levels early in the disease course of MS. Chromatolytic neurons and immunoreactivity for c-Jun and GAP43 were observed in the ventral gray matter in and adjacent to actively demyelinating lesions, pointing toward neuronal damage and regeneration as an early response to lesion formation."],["dc.identifier.doi","10.1002/ana.21799"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60301"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Substantial early, but nonprogressive neuronal loss in multiple sclerosis (ms) spinal cord"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3170"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","3183"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Blazquez, Raquel"],["dc.contributor.author","Rietkötter, Eva"],["dc.contributor.author","Wenske, Britta"],["dc.contributor.author","Wlochowitz, Darius"],["dc.contributor.author","Sparrer, Daniela"],["dc.contributor.author","Vollmer, Elena"],["dc.contributor.author","Müller, Gunnar"],["dc.contributor.author","Seegerer, Julia"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Barrantes‐Freer, Alonso"],["dc.contributor.author","Stange, Lena"],["dc.contributor.author","Utpatel, Kirsten"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Reimelt, Christian"],["dc.contributor.author","Hackl, Christina"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Büyüktas, Deram"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Balkenhol, Marko"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Krahn, Michael P."],["dc.contributor.author","Proescholdt, Martin A."],["dc.contributor.author","Riemenschneider, Markus J."],["dc.contributor.author","Evert, Matthias"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Klein, Chistoph A."],["dc.contributor.author","Hanisch, Uwe K."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-12-09T11:26:05Z"],["dc.date.accessioned","2021-10-27T13:21:49Z"],["dc.date.available","2019-12-09T11:26:05Z"],["dc.date.available","2021-10-27T13:21:49Z"],["dc.date.issued","2020"],["dc.description.abstract","More than half of all brain metastases show infiltrating rather than displacing growth at the macro-metastasis/organ parenchyma interface (MMPI), a finding associated with shorter survival. The lymphoid enhancer-binding factor-1 (LEF1) is an epithelial-mesenchymal transition (EMT) transcription factor that is commonly overexpressed in brain-colonizing cancer cells. Here, we overexpressed LEF1 in an in vivo breast cancer brain colonization model. It shortened survival, albeit without engaging EMT at the MMPI. By differential proteome analysis, we identified a novel function of LEF1 as a regulator of the glutathione (GSH) system, the principal cellular redox buffer. LEF1 overexpression also conferred resistance against therapeutic GSH depletion during brain colonization and improved management of intracellular ROS. We conclude that besides EMT, LEF1 facilitates metastasis by improving the antioxidative capacity of epithelial breast cancer cells, in particular during colonization of the brain parenchyma."],["dc.identifier.doi","10.1002/ijc.32742"],["dc.identifier.eissn","1097-0215"],["dc.identifier.issn","0020-7136"],["dc.identifier.pmid","31626715"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92047"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1097-0215"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]