Lühder, Fred

[["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.journal","Neurology"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Fluegel, Alexander"],["dc.date.accessioned","2018-11-07T09:11:32Z"],["dc.date.available","2018-11-07T09:11:32Z"],["dc.date.issued","2012"],["dc.identifier.isi","000303204801256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26744"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","64th Annual Meeting of the American-Academy-of-Neurology (AAN)"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0028-3878"],["dc.title","Analysis of Laquinimod Efficiency during Experimental Autoimmune Encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","2"],["dc.bibliographiccitation.volume","192"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:48:55Z"],["dc.date.available","2018-11-07T10:48:55Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1016/j.jneuroim.2007.10.011"],["dc.identifier.isi","000252163200001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48312"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Many roads lead to Rome: Heterogeneity among encephalitogenic T cell clones"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","397"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","406"],["dc.bibliographiccitation.volume","211"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Weller, Charlotte"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Schmidt, Jens"],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Metselaar, Josbert M."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T11:14:26Z"],["dc.date.available","2018-11-07T11:14:26Z"],["dc.date.issued","2008"],["dc.description.abstract","Liposomal encapsulation leads to enhanced efficacy of glucocorticosteroids (GS) in treatment of autoimmune diseases. Here we compare liposomal prednisolone (PL) to liposomal methylprednisolone (MPL) in chronic-relapsing myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE), a model closely reflecting aspects of multiple sclerosis (MS). At the maximum of the first relapse, a single dose of PL or MPL was applied at 10 mg/kg or at 4 mg/kg and compared to classical methylprednisolone (MP) pulse therapy. PL at 10 mg/kg was superior to free MP with long-term efficacy and a sustained protection even during the second and third relapse. At the same time, in vivo magnetic resonance imaging of rat brains revealed a significant reduction of T2-lesions after PL application. Comparison of PL and MPL at 10 mg/kg disclosed superior effects for MPL with an enhanced reduction of inflammatory infiltration as well as preservation of myelin and axons. Dose titration experiments underscored a dose-dependent efficacy of liposomal GS with a sustained efficacy especially of the higher dosage. In histological analyses, PL10 was superior in reducing macrophage and T cell infiltration as well as demyelination and axonal loss while the lower dosages were still at least as effective as free MP. FACS analyses revealed an effect of liposome formulations on T cell numbers, the CD4/CD8 ratio, frequencies of regulatory T cells and adhesion molecule expression. In summary, liposomal GS and especially methylprednisolone formulations display an enhanced efficacy not only in acute inflammatory, but also in chronic demyelinating models of MS and confer long-term protection from relapses. These findings lay the groundwork for applying liposomal GS in clinical MS trials in the near future. (c) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2008.02.005"],["dc.identifier.isi","000256272800012"],["dc.identifier.pmid","18394606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54122"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0014-4886"],["dc.title","Liposomal glucocorticosteroids in treatment of chronic autoimmune demyelination: Long-term protective effects and enhanced efficacy of methylprednisolone formulations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","7"],["dc.bibliographiccitation.volume","217"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Stegbauer, Johannes"],["dc.contributor.author","Linker, Ralf Andreas"],["dc.date.accessioned","2018-11-07T11:21:07Z"],["dc.date.available","2018-11-07T11:21:07Z"],["dc.date.issued","2009"],["dc.description.abstract","In the recent years, it has become increasingly clear that the immune response is also influenced by mediators which were first discovered as regulators in the nervous or also cardiovascular system. Here, small peptide hormones may play an important role. Kinins like bradykinins act on the endothelium and play a role for trafficking of lymphocytes over the blood-brain barrier. Neuropeptides like vasoactive intestinal peptide or neuropeptide Y also directly act on T cells and favour the differentiation of Th2 cells or regulatory T cell populations. Recently, the renin-angiotensin system (RAS) came into the focus of interest. Inhibition of the RAS at different levels may influence autoimmune responses and involve T cells as well as antigen-presenting cells, probably via different signalling pathways. Inhibitors of angiotensin converting enzyme and antagonists of the angiotensin I receptors are used in the treatment of hypertension, kidney disease or stroke by millions of people worldwide. These inexpensive and safe pharmaceuticals may also represent an interesting and innovative approach for the (combination) treatment of autoimmune diseases like multiple sclerosis. (C) 2009 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2009.08.008"],["dc.identifier.isi","000272896700001"],["dc.identifier.pmid","19748684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55698"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Small but powerful: Short peptide hormones and their role in autoimmune inflammation"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Clinical Immunology"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Schilling, S."],["dc.contributor.author","Goelz, S."],["dc.contributor.author","Linker, Ralf Andreas"],["dc.contributor.author","Luhder, F."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T08:36:16Z"],["dc.date.available","2018-11-07T08:36:16Z"],["dc.date.issued","2005"],["dc.format.extent","S88"],["dc.identifier.isi","000229104400244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18269"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.publisher.place","San diego"],["dc.relation.conference","5th Annual Meeting of the Federation-of-Clinical-Immunology-Society"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","1521-6616"],["dc.title","Fumarate therapy ameloriates chronic experimental autoimmune encephalomyelitis (EAE)."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","1914"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1925"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Frank, T."],["dc.contributor.author","Klinker, F."],["dc.contributor.author","Falkenburger, B. H."],["dc.contributor.author","Laage, R."],["dc.contributor.author","Lühder, F."],["dc.contributor.author","Göricke, B."],["dc.contributor.author","Schneider, A."],["dc.contributor.author","Neurath, H."],["dc.contributor.author","Desel, H."],["dc.contributor.author","Liebetanz, D."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Weishaupt, J. H."],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Recent proof-of-principle data showed that the haematopoietic growth factor granulocyte colony-stimulating factor (filgrastim) mediates neuroprotection in rodent models of Parkinson's disease. In preparation for future clinical trials, we performed a preclinical characterization of a pegylated derivative of granulocyte colony-stimulating factor (pegfilgrastim) in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease. We determined serum and cerebrospinal fluid drug levels after subcutaneous injection. A single injection of pegfilgrastim was shown to achieve stable levels of granulocyte colony-stimulating factor in both serum and cerebrospinal fluid with substantially higher levels compared to repetitive filgrastim injections. Leucocyte blood counts were only transiently increased after repeated injections. We demonstrated substantial dose-dependent long-term neuroprotection by pegfilgrastim in both young and aged mice, using bodyweight-adjusted doses that are applicable in clinical settings. Importantly, we found evidence for the functionally relevant preservation of nigrostriatal projections by pegfilgrastim in our model of Parkinson's disease, which resulted in improved motor performance. The more stable levels of pegylated neuroprotective proteins in serum and cerebrospinal fluid may represent a general advantage in the treatment of chronic neurodegenerative diseases and the resulting longer injection intervals are likely to improve patient compliance. In summary, we found that pegylation of a neuroprotective growth factor improved its pharmacokinetic profile over its non-modified counterpart in an in vivo model of Parkinson's disease. As the clinical safety profile of pegfilgrastim is already established, these data suggest that evaluation of pegfilgrastim in further Parkinson's disease models and ultimately clinical feasibility studies are warranted."],["dc.identifier.doi","10.1093/brain/aws054"],["dc.identifier.gro","3142529"],["dc.identifier.isi","000304538900022"],["dc.identifier.pmid","22427327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8890"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Michael J. Fox Foundation"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0006-8950"],["dc.subject","granulocyte colony-stimulating factor; 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; neuroprotection; Parkinson’s disease"],["dc.title","Pegylated granulocyte colony-stimulating factor conveys long-term neuroprotection and improves functional outcome in a model of Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]