Strauß, Judith

[["dc.bibliographiccitation.firstpage","1977"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","1990"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Li, Zhilin"],["dc.contributor.author","Korhonen, Emilia A."],["dc.contributor.author","Merlini, Arianna"],["dc.contributor.author","Strauss, Judith"],["dc.contributor.author","Wihuri, Eleonoora"],["dc.contributor.author","Nurmi, Harri"],["dc.contributor.author","Antila, Salli"],["dc.contributor.author","Paech, Jennifer"],["dc.contributor.author","Deutsch, Urban"],["dc.contributor.author","Engelhardt, Britta"],["dc.contributor.author","Chintharlapalli, Sudhakar"],["dc.contributor.author","Koh, Gou Young"],["dc.contributor.author","Flügel, Alexander"],["dc.contributor.author","Alitalo, Kari"],["dc.date.accessioned","2020-12-10T18:38:18Z"],["dc.date.available","2020-12-10T18:38:18Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1172/JCI130308"],["dc.identifier.eissn","1558-8238"],["dc.identifier.issn","0021-9738"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77266"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Angiopoietin-2 blockade ameliorates autoimmune neuroinflammation by inhibiting leukocyte recruitment into the CNS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","567"],["dc.bibliographiccitation.volume","140"],["dc.contributor.author","Hauptmann, Judith"],["dc.contributor.author","Johann, Lisa"],["dc.contributor.author","Marini, Federico"],["dc.contributor.author","Kitic, Maja"],["dc.contributor.author","Colombo, Elisa"],["dc.contributor.author","Mufazalov, Ilgiz A."],["dc.contributor.author","Krueger, Martin"],["dc.contributor.author","Karram, Khalad"],["dc.contributor.author","Moos, Sonja"],["dc.contributor.author","Wanke, Florian"],["dc.contributor.author","Kurschus, Florian C."],["dc.contributor.author","Klein, Matthias"],["dc.contributor.author","Cardoso, Silvia"],["dc.contributor.author","Strauß, Judith"],["dc.contributor.author","Bolisetty, Subhashini"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Schwaninger, Markus"],["dc.contributor.author","Binder, Harald"],["dc.contributor.author","Bechman, Ingo"],["dc.contributor.author","Bopp, Tobias"],["dc.contributor.author","Agarwal, Anupam"],["dc.contributor.author","Soares, Miguel P."],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Waisman, Ari"],["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/s00401-020-02187-x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81420"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood–brain barrier"],["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"]]

[["dc.bibliographiccitation.artnumber","49"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Ott, Martina"],["dc.contributor.author","Avendaño-Guzmán, Erika"],["dc.contributor.author","Ullrich, Evelyn"],["dc.contributor.author","Dreyer, Carolin"],["dc.contributor.author","Strauss, Judith"],["dc.contributor.author","Harden, Markus"],["dc.contributor.author","Schön, Margarete"],["dc.contributor.author","Schön, Michael P"],["dc.contributor.author","Bernhardt, Günter"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Nessler, Stefan"],["dc.date.accessioned","2019-07-09T11:50:03Z"],["dc.date.available","2019-07-09T11:50:03Z"],["dc.date.issued","2019"],["dc.description.abstract","Abstract Background Quinoline-3-carboxamides, such as laquinimod, ameliorate CNS autoimmunity in patients and reduce tumor cell metastasis experimentally. Previous studies have focused on the immunomodulatory effect of laquinimod on myeloid cells. The data contained herein suggest that quinoline-3-carboxamides improve the immunomodulatory and anti-tumor effects of NK cells by upregulating the adhesion molecule DNAX accessory molecule-1 (DNAM-1). Methods We explored how NK cell activation by laquinimod inhibits CNS autoimmunity in experimental autoimmune encephalomyelitis (EAE), the most utilized model of MS, and improves immunosurveillance of experimental lung melanoma metastasis. Functional manipulations included in vivo NK and DC depletion experiments and in vitro assays of NK cell function. Clinical, histological, and flow cytometric read-outs were assessed. Results We demonstrate that laquinimod activates natural killer (NK) cells via the aryl hydrocarbon receptor and increases their DNAM-1 cell surface expression. This activation improves the cytotoxicity of NK cells against B16F10 melanoma cells and augments their immunoregulatory functions in EAE by interacting with CD155+ dendritic cells (DC). Noteworthy, the immunosuppressive effect of laquinimod-activated NK cells was due to decreasing MHC class II antigen presentation by DC and not by increasing DC killing. Conclusions This study clarifies how DNAM-1 modifies the bidirectional crosstalk of NK cells with CD155+ DC, which can be exploited to suppress CNS autoimmunity and strengthen tumor surveillance."],["dc.identifier.doi","10.1186/s12974-019-1437-0"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15844"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59689"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","BioMed Central"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Laquinimod, a prototypic quinoline-3-carboxamide and aryl hydrocarbon receptor agonist, utilizes a CD155-mediated natural killer/dendritic cell interaction to suppress CNS autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.journal","Journal of Controlled Release"],["dc.bibliographiccitation.lastpage","169"],["dc.bibliographiccitation.volume","245"],["dc.contributor.author","Montes-Cobos, Elena"],["dc.contributor.author","Ring, Sarah"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Heck, Joachim G."],["dc.contributor.author","Strauss, Judith"],["dc.contributor.author","Schwaninger, Markus"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Feldmann, Claus"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:28:25Z"],["dc.date.available","2018-11-07T10:28:25Z"],["dc.date.issued","2017"],["dc.description.abstract","Glucocorticoids (GC) are widely used to treat acute relapses in multiple sclerosis (MS) patients, but their application is accompanied by side effects due to their broad spectrum of action. Here, we report on the therapeutic option to apply GC via inorganic-organic hybrid nanoparticles (IOH-NP) with the composition [ZrO](2+)[(BMP)(0.9)(FMN)(0.1)](2-) (designated BMP-NP with BMP: betamethasone phosphate; FMN: flavinmononucleotide). We found that these BMP-NP have an increased cell type-specificity compared to free GC while retaining full therapeutic efficacy in a mouse model of MS. BMP-NP were preferentially taken up by phagocytic cells and modulated macrophages in vivo more efficiently than T cells. When GC were applied in the form of BMP-NP, treatment of neuroinflammatory disease in mice exclusively depended on the control of macrophage function whereas effects on T cells and brain endothelial cells were dispensable for therapeutic efficacy. Importantly, BMP-NP were not only active in mice but also showed strong activity towards monocytes isolated from healthy human volunteers. We conclude that application of GC via IOH-NP has the potential to improve MS therapy in the future. (C) 2016 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","German Research Foundation (DFG) [RE 1631/15-1, LU 634/9-1]"],["dc.identifier.doi","10.1016/j.jconrel.2016.12.003"],["dc.identifier.isi","000396474500015"],["dc.identifier.pmid","27919626"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43416"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-4995"],["dc.relation.issn","0168-3659"],["dc.title","Targeted delivery of glucocorticoids to macrophages in a mouse model of multiple sclerosis using inorganic-organic hybrid nanoparticles"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]