Reichardt, Holger Michael

[["dc.bibliographiccitation.firstpage","48"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","61"],["dc.bibliographiccitation.volume","199"],["dc.contributor.author","Klaßen, Carina"],["dc.contributor.author","Karabinskaya, Anna"],["dc.contributor.author","Dejager, Lien"],["dc.contributor.author","Vettorazzi, Sabine"],["dc.contributor.author","Van Moorleghem, Justine"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Meijsing, Sebastiaan H."],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Libert, Claude"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2020-12-10T18:47:42Z"],["dc.date.available","2020-12-10T18:47:42Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.4049/jimmunol.1601691"],["dc.identifier.eissn","1550-6606"],["dc.identifier.issn","0022-1767"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78852"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1319"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Montes-Cobos, Elena"],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Li, Xiao"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.date.accessioned","2019-07-09T11:44:30Z"],["dc.date.available","2019-07-09T11:44:30Z"],["dc.date.issued","2017"],["dc.description.abstract","Myeloid cells play an important role in the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Monocytes, macrophages, and microglia can adopt two distinct phenotypes, with M1-polarized cells being more related to inflammation and autoimmunity while M2-polarized cells contribute to tissue repair and anti-inflammatory processes. Here, we show that deletion of the mineralocorticoid receptor (MR) in bone marrow-derived macrophages and peritoneal macrophages caused their polarization toward the M2 phenotype with its distinct gene expression, altered phagocytic and migratory properties, and dampened NO production. After induction of EAE, mice that are selectively devoid of the MR in their myeloid cells (MRlysM mice) showed diminished clinical symptoms and ameliorated histological hallmarks of neuroinflammation. T cells in peripheral lymphoid organs of these mice produced less pro-inflammatory cytokines while their proliferation and the abundance of regulatory T cells were unaltered. The numbers of inflammatory monocytes and reactive microglia in the central nervous system (CNS) in MRlysM mice were significantly lower and they adopted an M2-polarized phenotype based on their gene expression profile, presumably explaining the ameliorated neuroinflammation. Our results indicate that the MR in myeloid cells plays a critical role for CNS autoimmunity, providing a rational to interfere with diseases such as MS by pharmacologically targeting this receptor."],["dc.identifier.doi","10.3389/fimmu.2017.01319"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14800"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59025"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-3224"],["dc.relation.issn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Deletion of the Mineralocorticoid Receptor in Myeloid Cells Attenuates Central Nervous System Autoimmunity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1083"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1099"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","John, Michael"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Borisch, Angela"],["dc.contributor.author","Boutin, Philippe"],["dc.contributor.author","Neumann, Konstantin"],["dc.contributor.author","Bremes, Vanessa"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Waetzig, Vicky"],["dc.contributor.author","Herdegen, Thomas"],["dc.contributor.author","Teismann, Peter"],["dc.contributor.author","Greig, Iain"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Rotshenker, Shlomo"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:56:53Z"],["dc.date.available","2018-11-07T09:56:53Z"],["dc.date.issued","2015"],["dc.description.abstract","The putative protein tyrosine kinase (PTK) inhibitor tyrphostin AG126 has proven beneficial in various models of inflammatory disease. Yet molecular targets and cellular mechanisms remained enigmatic. We demonstrate here that AG126 treatment has beneficial effects in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. AG126 alleviates the clinical symptoms, diminishes encephalitogenic Th17 differentiation, reduces inflammatory CNS infiltration as well as microglia activation and attenuates myelin damage. We show that AG126 directly inhibits Bruton's tyrosine kinase (BTK), a PTK associated with B cell receptor and Toll-like receptor (TLR) signaling. However, BTK inhibition cannot account for the entire activity spectrum. Effects on TLR-induced proinflammatory cytokine expression in microglia involve AG126 hydrolysis and conversion of its dinitrile side chain to malononitrile (MN). Notably, while liberated MN can subsequently mediate critical AG126 features, full protection in EAE still requires delivery of intact AG126. Its anti-inflammatory potential and especially interference with TLR signaling thus rely on a dual mechanism encompassing BTK and a novel MN-sensitive target. Both principles bear great potential for the therapeutic management of disturbed innate and adaptive immune functions. GLIA 2015;63:1083-1099"],["dc.identifier.doi","10.1002/glia.22803"],["dc.identifier.isi","000353244400011"],["dc.identifier.pmid","25731696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37056"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Tyrphostin AG126 Exerts Neuroprotection in CNS Inflammation by a Dual Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","255"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Critical Reviews in Immunology"],["dc.bibliographiccitation.lastpage","273"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Luhder, Fred"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2021-06-01T10:48:29Z"],["dc.date.available","2021-06-01T10:48:29Z"],["dc.date.issued","2009"],["dc.description.abstract","Glucocorticoids (GCs) constitute one of the oldest families of anti-inflammatory and immunosuppressive drugs. Since their first clinical use more than half a century ago, they have been employed for therapeutic invention in a variety of conditions, including atopic disorders, autoimmune diseases, and cancer. Nevertheless, their exact mechanism of action is still incompletely understood. In this review, we elaborate especially on the mechanism of GCs in experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), and summarize our current knowledge on how therapeutic and endogenous GCs impact the pathogenesis of EAE and MS. This includes findings obtained from genetically modified mice and rats lacking or overexpressing the GC receptor (GR) in specific cell types, and the analysis of new pharmaceutical formulations and chemical GC modifications aimed at improving treatment efficacy and specificity. Stimulated by these recent developments, it can be anticipated that novel therapeutic regimens will find their way into clinical practice for the benefit of affected patients."],["dc.identifier.doi","10.1615/CritRevImmunol.v29.i3.50"],["dc.identifier.isi","000267432500005"],["dc.identifier.pmid","19538138"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85952"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Begell House Inc"],["dc.relation.issn","2162-6472"],["dc.relation.issn","1040-8401"],["dc.title","Traditional Concepts and Future Avenues of Glucocorticoid Action in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis Therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","John, Michael"],["dc.contributor.author","Neumann, K."],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Rotshenker, Shlomo"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T11:23:41Z"],["dc.date.available","2018-11-07T11:23:41Z"],["dc.date.issued","2009"],["dc.format.extent","S66"],["dc.identifier.isi","000270075500275"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56240"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.publisher.place","Hoboken"],["dc.relation.conference","9th European Meeting on Glial Cells in Health and Disease"],["dc.relation.eventlocation","Paris, FRANCE"],["dc.relation.issn","0894-1491"],["dc.title","TYRPHOSTIN AG126 MODULATES TOLL-LIKE RECEPTOR (TLR)-ACTIVATED RESPONSES IN MICROGLIA"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","99"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Molecular and Cellular Endocrinology"],["dc.bibliographiccitation.lastpage","107"],["dc.bibliographiccitation.volume","380"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T09:17:40Z"],["dc.date.available","2018-11-07T09:17:40Z"],["dc.date.issued","2013"],["dc.description.abstract","Glucocorticoids (GCs) are the most commonly prescribed drugs for the treatment of acute disease bouts in multiple sclerosis (MS) patients. While T lymphocytes were shown to be essential targets of GC therapy, at least in animal models of MS, the mechanisms by which GCs modulate T cell function are less clear. Until now, apoptosis induction and repression of pro-inflammatory cytokines in T cells have been considered the most critical mechanisms in ameliorating disease symptoms. However, this notion is being challenged by increasing evidence that the control of T cell migration and chemotaxis by GCs might be even more important for the treatment of neuroinflammatory diseases. In this review we aim to provide an overview of how GCs impact the morphological alterations that T cells undergo during activation and migration as well as the influences that GCs have on the directed movement of T cells under the influence of chemokines. A deeper understanding of these processes should not only help to advance our understanding of how GCs exert their beneficial effects in MS therapy but may reveal future strategies to intervene in the pathogenesis of neuroinflammatory diseases. (C) 2013 Elsevier Ireland Ltd. All rights reserved."],["dc.description.sponsorship","DFG [Lu634/8-1, SFB-TRR 43/B11, SFB-TRR 43/B13]"],["dc.identifier.doi","10.1016/j.mce.2013.04.001"],["dc.identifier.isi","000326912400011"],["dc.identifier.pmid","23578583"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28221"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0303-7207"],["dc.title","The potential role of T cell migration and chemotaxis as targets of glucocorticoids in multiple sclerosis and experimental autoimmune encephalomyelitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bier, Jasmina"],["dc.contributor.author","Steiger, Sebastian M."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.date.accessioned","2021-07-05T14:57:53Z"],["dc.date.available","2021-07-05T14:57:53Z"],["dc.date.issued","2021"],["dc.description.abstract","Induction of T cell apoptosis constitutes a major mechanism by which therapeutically administered glucocorticoids (GCs) suppress inflammation and associated clinical symptoms, for instance in multiple sclerosis (MS) patients suffering from an acute relapse. The sensitivity of T cells to GC action depends on their maturation and activation status, but the precise effect of antigen-priming in a pathological setting has not been explored. Here we used transgenic and congenic mouse models to compare GC-induced apoptosis between naïve and antigen-specific effector T cells from mice immunized with a myelin peptide. Antigen-primed effector T cells were protected from the pro-apoptotic activity of the synthetic GC dexamethasone in a dose-dependent manner, which resulted in their accumulation relative to naïve T cells in vitro and in vivo . Notably, the differential sensitivity of T cells to GC-induced apoptosis correlated with their expression level of the anti-apoptotic proteins Bcl-2 and Bcl-X L and a loss of the mitochondrial membrane potential. Moreover, accumulation of antigen-primed effector T cells following GC treatment in vitro resulted in an aggravated disease course in an adoptive transfer mouse model of MS in vivo , highlighting the clinical relevance of the observed phenomenon. Collectively, our data indicate that antigen-priming influences the T cells’ sensitivity to therapeutically applied GCs in the context of inflammatory diseases."],["dc.description.abstract","Induction of T cell apoptosis constitutes a major mechanism by which therapeutically administered glucocorticoids (GCs) suppress inflammation and associated clinical symptoms, for instance in multiple sclerosis (MS) patients suffering from an acute relapse. The sensitivity of T cells to GC action depends on their maturation and activation status, but the precise effect of antigen-priming in a pathological setting has not been explored. Here we used transgenic and congenic mouse models to compare GC-induced apoptosis between naïve and antigen-specific effector T cells from mice immunized with a myelin peptide. Antigen-primed effector T cells were protected from the pro-apoptotic activity of the synthetic GC dexamethasone in a dose-dependent manner, which resulted in their accumulation relative to naïve T cells in vitro and in vivo . Notably, the differential sensitivity of T cells to GC-induced apoptosis correlated with their expression level of the anti-apoptotic proteins Bcl-2 and Bcl-X L and a loss of the mitochondrial membrane potential. Moreover, accumulation of antigen-primed effector T cells following GC treatment in vitro resulted in an aggravated disease course in an adoptive transfer mouse model of MS in vivo , highlighting the clinical relevance of the observed phenomenon. Collectively, our data indicate that antigen-priming influences the T cells\\’ sensitivity to therapeutically applied GCs in the context of inflammatory diseases."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fimmu.2021.671258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87763"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-441"],["dc.relation.eissn","1664-3224"],["dc.relation.orgunit","Institut für Neuroimmunologie und Multiple-Sklerose-Forschung"],["dc.rights","CC BY 4.0"],["dc.title","Protection of Antigen-Primed Effector T Cells From Glucocorticoid-Induced Apoptosis in Cell Culture and in a Mouse Model of Multiple Sclerosis"],["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","2921"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.affiliation","Reichardt, Sybille D.; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Amouret, Agathe; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Muzzi, Chiara; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Vettorazzi, Sabine; 2Institute of Comparative Molecular Endocrinology, Ulm University, 89081 Ulm, Germany; sabine.vettorazzi@uni-ulm.de (S.V.); jan.tuckermann@uni-ulm.de (J.P.T.)"],["dc.contributor.affiliation","Tuckermann, Jan P.; 2Institute of Comparative Molecular Endocrinology, Ulm University, 89081 Ulm, Germany; sabine.vettorazzi@uni-ulm.de (S.V.); jan.tuckermann@uni-ulm.de (J.P.T.)"],["dc.contributor.affiliation","Lühder, Fred; 3Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany; fred.luehder@med.uni-goettingen.de"],["dc.contributor.affiliation","Reichardt, Holger M.; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Amouret, Agathe"],["dc.contributor.author","Muzzi, Chiara"],["dc.contributor.author","Vettorazzi, Sabine"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2022-01-11T14:07:51Z"],["dc.date.available","2022-01-11T14:07:51Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:20:27Z"],["dc.description.abstract","For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use."],["dc.description.abstract","For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/cells10112921"],["dc.identifier.eissn","2073-4409"],["dc.identifier.pii","cells10112921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97878"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2073-4409"],["dc.relation.orgunit","Institut für Zelluläre und Molekulare Immunologie"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","The Role of Glucocorticoids in Inflammatory Diseases"],["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","174"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroendocrinology"],["dc.bibliographiccitation.lastpage","182"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T09:15:58Z"],["dc.date.available","2018-11-07T09:15:58Z"],["dc.date.issued","2012"],["dc.description.abstract","Glucocorticoids (GCs) are widely used to treat inflammatory diseases such as multiple sclerosis (MS). They predominantly act through the GC receptor, a member of the nuclear receptor superfamily that controls transcription by several different mechanisms. Owing to its ubiquitous expression, there are a variety of cell types that could serve as GC targets in the pathogenesis and treatment of MS. This brings about a great diversity of mechanisms potentially involved in the modulation of neuroinflammation by GCs, including the induction of apoptosis, repression of pro-inflammatory mediators and the expansion of myeloid-derived suppressor cells. Nevertheless, it is not well understood which of these mechanisms are essential for therapeutic efficacy. In this review, we summarise findings made concerning the actions of GCs in MS and its animal model experimental autoimmune encephalomyelitis, and also elucidate current concepts and developments that pertain to this clinically highly relevant treatment regimen."],["dc.identifier.doi","10.1111/j.1365-2826.2011.02161.x"],["dc.identifier.isi","000298601800016"],["dc.identifier.pmid","21615563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27832"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0953-8194"],["dc.title","Mechanisms of Glucocorticoids in the Control of Neuroinflammation"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Stadeimann, Christine"],["dc.date.accessioned","2018-11-07T11:11:44Z"],["dc.date.available","2018-11-07T11:11:44Z"],["dc.date.issued","2008"],["dc.format.extent","S79"],["dc.identifier.isi","000259675700247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53499"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","13th Annual Meeting of the Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th Congress of the Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Montreal, CANADA"],["dc.relation.issn","1352-4585"],["dc.title","Experimental autoimmune encephalomyelitis induction in mice with cuprizone-induced demyelination leads to cerebral MS-like lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]