Gold, Ralf

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical & Experimental Immunology"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Hofstetter, Harald H."],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Lesch, K. P."],["dc.contributor.author","Linker, Ralf Andreas"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:55:12Z"],["dc.date.available","2018-11-07T10:55:12Z"],["dc.date.issued","2005"],["dc.description.abstract","Serotonin (5-hydroxytryptamine, 5-HT) is one of the most extensively studied neurotransmitters of the central nervous system. It also has been identified in constituents of the immune system. Therefore serotonin has been suggested to serve as a mediator of bidirectional interactions between the nervous system and the immune system. We investigated this interaction in experimental autoimmune encephalomyelitis (EAE), a well-defined animal model of autoimmune disease of the central nervous system (CNS) mimicking features of the human disease multiple sclerosis. EAE was induced by immunization with the autoantigens myelin basic protein (MBP) or the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) spanning amino acids 35-55 (MOGp 35-55). We studied EAE in knockout (KO) mice lacking the 5-HT transporter (5-HTT) on a C57.BL/6 background, in comparison with wild-type C57.BL/6 animals. After immunization with MOGp 35-55, or with rat MBP, the disease courses of the 5-HTT knockout mice were attenuated as compared to wildtype control mice. This difference was more pronounced in female animals. To dissect potential immune mechanisms underlying this phenomenon, histological studies of the CNS and cytokine measurements in mononuclear cells from the spleens of 5-HTT KO mice and wild-type controls were performed. We found a reduction of the inflammatory infiltrate in the CNS and of the neuroantigen-specific production of IFN-gamma in splenocytes, again accompanied by a gender difference. These findings suggest a potential role of extracellular 5-HT homeostasis in the fine-tuning of neuroantigen-specific immune responses."],["dc.identifier.doi","10.1111/j.1365-2249.2005.02901.X"],["dc.identifier.isi","000231824900005"],["dc.identifier.pmid","16178854"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49732"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0009-9104"],["dc.title","Absence of reuptake of serotonin influences susceptibility to clinical autoimmune disease and neuroantigen-specific interferon-gamma production in mouse EAE"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","678"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","692"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Ryan, Sarah"],["dc.contributor.author","van Dam, Anne M."],["dc.contributor.author","Conrad, Rebecca"],["dc.contributor.author","Bista, Pradeep"],["dc.contributor.author","Zeng, Weike"],["dc.contributor.author","Hronowsky, Xiaoping"],["dc.contributor.author","Buko, Alex"],["dc.contributor.author","Chollate, Sowmya"],["dc.contributor.author","Ellrichmann, Gisa"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Dawson, Kate"],["dc.contributor.author","Goelz, Susan"],["dc.contributor.author","Wiese, Stefan"],["dc.contributor.author","Scannevin, Robert H."],["dc.contributor.author","Lukashev, Matvey"],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T08:59:01Z"],["dc.date.available","2018-11-07T08:59:01Z"],["dc.date.issued","2011"],["dc.description.abstract","Inflammation and oxidative stress are thought to promote tissue damage in multiple sclerosis. Thus, novel therapeutics enhancing cellular resistance to free radicals could prove useful for multiple sclerosis treatment. BG00012 is an oral formulation of dimethylfumarate. In a phase II multiple sclerosis trial, BG00012 demonstrated beneficial effects on relapse rate and magnetic resonance imaging markers indicative of inflammation as well as axonal destruction. First we have studied effects of dimethylfumarate on the disease course, central nervous system, tissue integrity and the molecular mechanism of action in an animal model of chronic multiple sclerosis: myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis in C57BL/6 mice. In the chronic phase of experimental autoimmune encephalomyelitis, preventive or therapeutic application of dimethylfumarate ameliorated the disease course and improved preservation of myelin, axons and neurons. In vitro, the application of fumarates increased murine neuronal survival and protected human or rodent astrocytes against oxidative stress. Application of dimethylfumarate led to stabilization of the transcription factor nuclear factor (erythroid-derived 2)-related factor 2, activation of nuclear factor (erythroid-derived 2)-related factor 2-dependent transcriptional activity and accumulation of NADP(H) quinoline oxidoreductase-1 as a prototypical target gene. Furthermore, the immediate metabolite of dimethylfumarate, monomethylfumarate, leads to direct modification of the inhibitor of nuclear factor (erythroid-derived 2)-related factor 2, Kelch-like ECH-associated protein 1, at cysteine residue 151. In turn, increased levels of nuclear factor (erythroid-derived 2)-related factor 2 and reduced protein nitrosylation were detected in the central nervous sytem of dimethylfumarate-treated mice. Nuclear factor (erythroid-derived 2)-related factor 2 was also upregulated in the spinal cord of autopsy specimens from untreated patients with multiple sclerosis. In dimethylfumarate-treated mice suffering from experimental autoimmune encephalomyelitis, increased immunoreactivity for nuclear factor (erythroid-derived 2)-related factor 2 was detected by confocal microscopy in neurons of the motor cortex and the brainstem as well as in oligodendrocytes and astrocytes. In mice deficient for nuclear factor (erythroid-derived 2)-related factor 2 on the same genetic background, the dimethylfumarate mediated beneficial effects on clinical course, axon preservation and astrocyte activation were almost completely abolished thus proving the functional relevance of this transcription factor for the neuroprotective mechanism of action. We conclude that the ability of dimethylfumarate to activate nuclear factor (erythroid-derived 2)-related factor 2 may offer a novel cytoprotective modality that further augments the natural antioxidant responses in multiple sclerosis tissue and is not yet targeted by other multiple sclerosis therapies."],["dc.description.sponsorship","Biogen Idec; Ruhr University Bochum"],["dc.identifier.doi","10.1093/brain/awq386"],["dc.identifier.isi","000287745100006"],["dc.identifier.pmid","21354971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23784"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Fumaric acid esters exert neuroprotective effects in neuroinflammation via activation of the Nrf2 antioxidant pathway"],["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","589"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","598"],["dc.bibliographiccitation.volume","171"],["dc.contributor.author","Herrero-Herranz, Eva"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2018-11-07T10:59:44Z"],["dc.date.available","2018-11-07T10:59:44Z"],["dc.date.issued","2007"],["dc.description.abstract","Mechanisms of lesion repair in multiple sclerosis are incompletely understood. To some degree, remyelination can occur, associated with an increase of proliferating oligodendroglial cells. Recently, the expression of potassium channels has been implicated in the control of oligodendrocyte precursor cell proliferation in vitro. We investigated the expression of Kv1.4 potassium channels in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Confocal microscopy revealed expression of Kv1.4 in AN2-positive oligodendrocyte precursor cells and pre-myelinating oligodendrocytes in vitro but neither in mature oligodendrocytes nor in the spinal cords of healthy adult mice. After induction of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, Kv1.4 immunoreactivity was detected in or around lesions already during disease onset with a peak early and a subsequent decrease in the late phase of the disease. Kv1.4 expression was confined to 2',3'-cyclic nucleotide 3'-phosphodiesterase-positive oligodendroglial cells, which were actively proliferating and ensheathed naked axons. After a demyelinating episode, the number of Kv1.4 and 2',3'-cyclic nucleotide 3'-phosphodiesterase double-positive cells was greatly reduced in ciliary neurotrophic factor knockout mice, a model with impaired lesion repair. in summary, the re-expression of an oligodendroglial potassium channel may have a functional implication on oligodendroglial cell cycle progression, thus influencing tissue repair in experimental autoimmune encephalomyelitis and multiple sclerosis."],["dc.identifier.doi","10.2353/ajpath.2007.061241"],["dc.identifier.isi","000248496300022"],["dc.identifier.pmid","17600124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50766"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0002-9440"],["dc.title","Re-expression of a developmentally restricted potassium channel in autoimmune demyelination - Kv1.4 is implicated in oligodendroglial proliferation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","715"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Fortschritte der Neurologie · Psychiatrie"],["dc.bibliographiccitation.lastpage","727"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Linker, R. A."],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Diem, R."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Brück, W."],["dc.contributor.author","Gold, R."],["dc.date.accessioned","2017-09-07T11:53:40Z"],["dc.date.available","2017-09-07T11:53:40Z"],["dc.date.issued","2005"],["dc.description.abstract","In this article, recent advances in the research on pathogenesis and therapy of multiple sclerosis (MS) will be summarized. New evidence from clinical studies, imaging, histopathology and experimental models are discussed with a focus on neurodegenerative aspects and evidence from recent therapeutic studies. During the last decade, important advances in immunotherapy have been achieved, which proved especially useful for patients with relapsing remitting MS. The introduction of interferons and glatiramer acetate into MS therapy often leads to a stabilization of the disease course if administered adequately and early. The pathogenetic insights presented here may open new avenues for innovative immunodulatory approaches and lead to an individualized MS therapy in the future. Neuroprotective treatment strategies aim at the protection of glial and neuronal cells."],["dc.description.abstract","In dieser Übersichtsarbeit stellen wir die in den letzten Jahren erzielten Fortschritte bei der Erforschung der Multiplen Sklerose dar und diskutieren sie kritisch. Aus klinischen, bildgebenden, pathologischen, immunologischen und tierexperimentellen Studien resultierten neue Erkenntnisse zur Pathogenese und Therapie der MS. Schwerpunkte liegen insbesondere auf neurodegenerativen Aspekten der Erkrankung sowie auf therapierelevanten Befunden, die bereits zu einer deutlichen Verbesserung der Immuntherapie im letzten Jahrzehnt führten. Vor allem bei der schubförmig verlaufenden MS kann seit der Einführung der Immunmodulation mit Interferonen und Glatiramerazetat in vielen Fällen die Krankheit durch adäquate und frühe Behandlung langfristig stabilisiert werden. In naher Zukunft sind neue Immuntherapeutika, aber wahrscheinlich auch individualisierte Behandlungsansätze zu erwarten. Die weitere Entwicklung neurobiologisch-protektiver Strategien soll gezielt das Überleben von Glia- und Nervenzellen fördern."],["dc.identifier.doi","10.1055/s-2004-830256"],["dc.identifier.gro","3143783"],["dc.identifier.isi","000234046600002"],["dc.identifier.pmid","16355314"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1335"],["dc.language.iso","de"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0720-4299"],["dc.title","Recent advances in pathogenesis and therapy of multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","325"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","332"],["dc.bibliographiccitation.volume","229"],["dc.contributor.author","Peruga, Isabella"],["dc.contributor.author","Hartwig, Silvia"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Thoene, Jan"],["dc.contributor.author","Hovemann, Bernhard"],["dc.contributor.author","Juckel, Georg"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2018-11-07T09:11:09Z"],["dc.date.available","2018-11-07T09:11:09Z"],["dc.date.issued","2012"],["dc.description.abstract","On a molecular level, depression is characterized by an altered monoaminergic neurotransmission as well as a modulation of cytokines and other mediators in the central nervous system. In particular, neurotrophic factors may influence affective behavior including depression and anxiety. Ciliary neurotrophic factor (CNTF) plays an important role in the regulation of neuronal development, neuroprotection and may also influence cognitive processes. Here we investigate the affective behavior in mice deficient for CNTF (CNTF -/- mice) at young age of 10-20 weeks. CNTF -/- mice displayed an increased anxiety-like behavior with a 30% reduction of the time spent in the bright compartment of the light/dark box as well as a significantly increased startle response. In the learned helplessness paradigm, CNTF -/- mice are more prone to depressive-like behavior. In the hippocampus of 20 weeks old, but not 10 weeks old, CNTF -/- mice, these changes correlated with a loss of parvalbumin immunoreactive GABAergic interneurons and a reduction of serotonin levels as well as 5-HT receptor 1A expression. Modulation of monoaminergic neurotransmitter levels via chronic application of the antidepressants amitriptyline and citalopram did not exert beneficial effects. These data imply that endogenous CNTF plays a pivotal role for the structural maintenance of hippocampal functions and thus has an important impact on the modulation of affective behavior in rodent models of anxiety and depression. (C) 2012 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.bbr.2012.01.020"],["dc.identifier.isi","000302050300004"],["dc.identifier.pmid","22266927"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26660"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0166-4328"],["dc.title","Endogenous ciliary neurotrophic factor modulates anxiety and depressive-like behavior"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","43"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Critical Reviews in Immunology"],["dc.bibliographiccitation.lastpage","68"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Luehder, Fred"],["dc.date.accessioned","2018-11-07T08:34:17Z"],["dc.date.available","2018-11-07T08:34:17Z"],["dc.date.issued","2009"],["dc.description.abstract","In the nervous system, neurotrophic factors play a role during development, especially for the differentiation of neuronal and glial cells. Moreover, they promote cell survival of neurons, axons, and oligodendrocytes, as well as their precursors, in vitro and in lesional paradigms. In recent years, several functions of neurotrophic factors outside the nervous system have been described, with a special focus on the immune system as well as on models of autoimmune demyelination, such as experimental autoimmune encephalomyelitis (EAE). In the family of neurotrophins, nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) were investigated. NGF may influence B-cell as well as T-cell function and particularly plays a role in macrophage migration into inflamed lesions. BDNF is produced by several immune-cell subtypes in vitro and also in multiple sclerosis (MS) plaques. This observation gave rise to the concept of neuroprotective autoimmunity, implying that immune-cell infiltration in the nervous system may not only be detrimental but may also play a beneficial role, for example, through the production of neurotrophic factors. In the family of neurotrophic cytokines, ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF) share some common protective roles in axons and oligodendrocytes. In EAE, endogenous CNTF targets myelin, oligodendroglial cells, and axons. In contrast, LIF exerts protective functions on oligodendrocytes in some models but is also able to interact with the immune response and may modulate T-cell, monocyte and neutrophil functions. In summary, neurotrophic factors have distinct roles in the immune system during autoimmunity and may modulate immune responses as well as the susceptibility of the target tissue."],["dc.identifier.isi","000265560700002"],["dc.identifier.pmid","19348610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17776"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Begell House Inc"],["dc.relation.issn","1040-8401"],["dc.title","Function of Neurotrophic Factors Beyond the Nervous System: Inflammation and Autoimmune Demyelination"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2248"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2263"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Demir, Seray"],["dc.contributor.author","Wiese, Stefan"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Siglienti, Ines"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Neumann, Harald"],["dc.contributor.author","Sendtner, Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T08:40:38Z"],["dc.date.available","2018-11-07T08:40:38Z"],["dc.date.issued","2010"],["dc.description.abstract","Brain-derived neurotrophic factor plays a key role in neuronal and axonal survival. Brain-derived neurotrophic factor is expressed in the immune cells in lesions of experimental autoimmune encephalomyelitis and multiple sclerosis, thus potentially mediating neuroprotective effects. We investigated the functional role of brain-derived neurotrophic factor in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Mice deficient for brain-derived neurotrophic factor in immune cells displayed an attenuated immune response in the acute phase of experimental autoimmune encephalomyelitis, but progressive disability with enhanced axonal loss in the chronic phase of the disease. In mice deficient for central nervous system-derived brain-derived neurotrophic factor via glial fibrillary acidic protein-crescentin-mediated deletion, a more severe course of experimental autoimmune encephalomyelitis and an overall increased axonal loss was observed. In a lentiviral approach, injection of brain-derived neurotrophic factor-overexpressing T cells led to a less severe course of experimental autoimmune encephalomyelitis and direct axonal protection. Our data imply a functional role of brain-derived neurotrophic factor in autoimmune demyelination by mediating axon protection."],["dc.identifier.doi","10.1093/brain/awq179"],["dc.identifier.isi","000280982700010"],["dc.identifier.pmid","20826430"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6203"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19277"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Functional role of brain-derived neurotrophic factor in neuroprotective autoimmunity: therapeutic implications in a model of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]