Pellkofer, Hannah Luise

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Siebert, Nadja"],["dc.contributor.author","Korporal-Kuhnke, Mirjam"],["dc.contributor.author","Hümmert, Martin W."],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Rommer, Paulus S."],["dc.contributor.author","Ayzenberg, Ilya"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Klotz, Luisa"],["dc.contributor.author","Asgari, Nasrin"],["dc.contributor.author","Zrzavy, Tobias"],["dc.contributor.author","Höftberger, Romana"],["dc.contributor.author","Tobia, Rafik"],["dc.contributor.author","Buttmann, Mathias"],["dc.contributor.author","Fechner, Kai"],["dc.contributor.author","Schanda, Kathrin"],["dc.contributor.author","Weber, Martin"],["dc.contributor.author","Asseyer, Susanna"],["dc.contributor.author","Haas, Jürgen"],["dc.contributor.author","Lechner, Christian"],["dc.contributor.author","Kleiter, Ingo"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Kümpfel, Tania"],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Wildemann, Brigitte"],["dc.date.accessioned","2021-04-14T08:32:46Z"],["dc.date.available","2021-04-14T08:32:46Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s12974-020-01824-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17535"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84009"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1742-2094"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid findings in patients with myelin oligodendrocyte glycoprotein (MOG) antibodies. Part 1: Results from 163 lumbar punctures in 100 adult patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Traub, Jan W."],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Grondey, Katja"],["dc.contributor.author","Seeger, Ira"],["dc.contributor.author","Rowold, Christoph"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Husseini, Leila"],["dc.contributor.author","Häusser-Kinzel, Silke"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-06-01T10:48:04Z"],["dc.date.available","2021-06-01T10:48:04Z"],["dc.date.issued","2019"],["dc.description.abstract","Abstract Background In the past, multiple sclerosis (MS) medications have been primarily designed to modulate T cell properties. Based on the emerging concept that B cells are equally important for the propagation of MS, we compared the effect of four commonly used, primarily T cell-targeting MS medications on B cells. Methods Using flow cytometry, we analyzed peripheral blood mononuclear cells (PBMC) of untreated ( n  = 19) and dimethyl fumarate (DMF; n  = 21)-, fingolimod (FTY; n  = 17)-, glatiramer acetate (GA; n  = 18)-, and natalizumab (NAT; n  = 20)-treated MS patients, focusing on B cell maturation, differentiation, and cytokine production. Results While GA exerted minor effects on the investigated B cell properties, DMF and FTY robustly inhibited pro-inflammatory B cell function. In contrast, NAT treatment enhanced B cell differentiation, activation, and pro-inflammatory cytokine production when compared to both intraindividual samples collected before NAT treatment initiation as well as untreated MS controls. Our mechanistic in vitro studies confirm this observation. Conclusion Our data indicate that common MS medications have differential, in part opposing effects on B cells. The observed activation of peripheral B cells upon NAT treatment may be instructive to interpret its unfavorable effect in certain B cell-mediated inflammatory conditions and to elucidate the immunological basis of MS relapses after NAT withdrawal. Trial registration Protocols were approved by the ethical review committee of the University Medical Center Göttingen (#3/4/14)."],["dc.identifier.doi","10.1186/s12974-019-1593-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85818"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Natalizumab promotes activation and pro-inflammatory differentiation of peripheral B cells in multiple sclerosis patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.journal","Cortex"],["dc.bibliographiccitation.lastpage","40"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Albrecht, Franziska"],["dc.contributor.author","Mueller, Karsten"],["dc.contributor.author","Ballarini, Tommaso"],["dc.contributor.author","Lampe, Leonie"],["dc.contributor.author","Diehl-Schmid, Janine"],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Jech, Robert"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Landwehrmeyer, Bernhard"],["dc.contributor.author","Lauer, Martin"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Lyros, Epameinondas"],["dc.contributor.author","Prudlo, Johannes"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Synofzik, Matthis"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Danek, Adrian"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Schroeter, Matthias L."],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Brüggen, Katharina"],["dc.contributor.author","Fischer, Marie"],["dc.contributor.author","Förstl, Hans"],["dc.contributor.author","Hammer, Anke"],["dc.contributor.author","Homola, György"],["dc.contributor.author","Just, Walter"],["dc.contributor.author","Levin, Johannes"],["dc.contributor.author","Marroquin, Nicolai"],["dc.contributor.author","Marschhauser, Anke"],["dc.contributor.author","Nagl, Magdalena"],["dc.contributor.author","Oberstein, Timo"],["dc.contributor.author","Polyakova, Maryna"],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Richter-Schmidinger, Tanja"],["dc.contributor.author","Rossmeier, Carola"],["dc.contributor.author","Schuemberg, Katharina"],["dc.contributor.author","Semler, Elisa"],["dc.contributor.author","Spottke, Annika"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Thöne-Otto, Angelika"],["dc.contributor.author","Uttner, Ingo"],["dc.contributor.author","Zech, Heike"],["dc.date.accessioned","2020-12-10T14:23:17Z"],["dc.date.available","2020-12-10T14:23:17Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.cortex.2019.02.015"],["dc.identifier.issn","0010-9452"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16567"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71890"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Unraveling corticobasal syndrome and alien limb syndrome with structural brain imaging"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e71500"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Havla, Joachim"],["dc.contributor.author","Hauer, Daniela"],["dc.contributor.author","Schelling, Gustav"],["dc.contributor.author","Azad, Shahnaz C."],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Magerl, Walter"],["dc.contributor.author","Huge, Volker"],["dc.date.accessioned","2018-11-07T09:21:20Z"],["dc.date.available","2018-11-07T09:21:20Z"],["dc.date.issued","2013"],["dc.description.abstract","Recurrent myelitis is one of the predominant characteristics in patients with neuromyelitis optica (NMO). While paresis, visual loss, sensory deficits, and bladder dysfunction are well known symptoms in NMO patients, pain has been recognized only recently as another key symptom of the disease. Although spinal cord inflammation is a defining aspect of neuromyelitis, there is an almost complete lack of data on altered somatosensory function, including pain. Therefore, eleven consecutive patients with NMO were investigated regarding the presence and clinical characteristics of pain. All patients were examined clinically as well as by Quantitative Sensory Testing (QST) following the protocol of the German Research Network on Neuropathic Pain (DFNS). Additionally, plasma endocannabinoid levels and signs of chronic stress and depression were determined. Almost all patients (10/11) suffered from NMO-associated neuropathic pain for the last three months, and 8 out of 11 patients indicated relevant pain at the time of examination. Symptoms of neuropathic pain were reported in the vast majority of patients with NMO. Psychological testing revealed signs of marked depression. Compared to age and gender-matched healthy controls, QST revealed pronounced mechanical and thermal sensory loss, strongly correlated to ongoing pain suggesting the presence of deafferentation-induced neuropathic pain. Thermal hyperalgesia correlated to MRI-verified signs of spinal cord lesion. Heat hyperalgesia was highly correlated to the time since last relapse of NMO. Patients with NMO exhibited significant mechanical and thermal dysesthesia, namely dynamic mechanical allodynia and paradoxical heat sensation. Moreover, they presented frequently with either abnormal mechanical hypoalgesia or hyperalgesia, which depended significantly on plasma levels of the endogenous cannabinoid 2-arachidonoylglycerole (2-AG). These data emphasize the high prevalence of neuropathic pain and hyperalgesia in patients with NMO. The degree of mechanical hyperalgesia reflecting central sensitization of nociceptive pathways seems to be controlled by the major brain endocannabinoid 2-AG."],["dc.identifier.doi","10.1371/journal.pone.0071500"],["dc.identifier.isi","000326473200051"],["dc.identifier.pmid","23951176"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9229"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29084"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","The Major Brain Endocannabinoid 2-AG Controls Neuropathic Pain and Mechanical Hyperalgesia in Patients with Neuromyelitis Optica"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Geis, Christian"],["dc.contributor.author","Kleiter, Ingo"],["dc.contributor.author","Kleinschnitz, Christoph"],["dc.contributor.author","Berthele, Achim"],["dc.contributor.author","Brettschneider, Johannes"],["dc.contributor.author","Hellwig, Kerstin"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lauda, Florian"],["dc.contributor.author","Mayer, Christoph A."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Melms, Arthur"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Stangel, Martin"],["dc.contributor.author","Marziniak, Martin"],["dc.contributor.author","Hoffmann, Frank"],["dc.contributor.author","Schippling, Sven"],["dc.contributor.author","Faiss, Juergen H."],["dc.contributor.author","Neuhaus, Oliver"],["dc.contributor.author","Ettrich, Barbara"],["dc.contributor.author","Zentner, Christian"],["dc.contributor.author","Guthke, Kersten"],["dc.contributor.author","Hofstadt-van Oy, Ulrich"],["dc.contributor.author","Reuss, Reinhard"],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Ziemann, Ulf"],["dc.contributor.author","Kern, Peter"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Bergh, Florian Then"],["dc.contributor.author","Boettcher, Tobias"],["dc.contributor.author","Langel, Stefan"],["dc.contributor.author","Liebetrau, Martin"],["dc.contributor.author","Rommer, Paulus S."],["dc.contributor.author","Niehaus, Sabine"],["dc.contributor.author","Muench, Christoph"],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl U, Uwe K."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Veauthier, Christian"],["dc.contributor.author","Sieb, Joern P."],["dc.contributor.author","Wilke, Christian"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Paul, Friedemann"],["dc.date.accessioned","2018-11-07T09:14:18Z"],["dc.date.available","2018-11-07T09:14:18Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: The diagnostic and pathophysiological relevance of antibodies to aquaporin-4 (AQP4-Ab) in patients with neuromyelitis optica spectrum disorders (NMOSD) has been intensively studied. However, little is known so far about the clinical impact of AQP4-Ab seropositivity. Objective: To analyse systematically the clinical and paraclinical features associated with NMO spectrum disorders in Caucasians in a stratified fashion according to the patients' AQP4-Ab serostatus. Methods: Retrospective study of 175 Caucasian patients (AQP4-Ab positive in 78.3%). Results: Seropositive patients were found to be predominantly female (p < 0.0003), to more often have signs of co-existing autoimmunity (p < 0.00001), and to experience more severe clinical attacks. A visual acuity of <= 0.1 during acute optic neuritis (ON) attacks was more frequent among seropositives (p < 0.002). Similarly, motor symptoms were more common in seropositive patients, the median Medical Research Council scale (MRC) grade worse, and MRC grades <= 2 more frequent, in particular if patients met the 2006 revised criteria (p < 0.005, p < 0.006 and p < 0.01, respectively), the total spinal cord lesion load was higher (p < 0.006), and lesions >= 6 vertebral segments as well as entire spinal cord involvement more frequent (p < 0.003 and p < 0.043). By contrast, bilateral ON at onset was more common in seronegatives (p < 0.007), as was simultaneous ON and myelitis (p < 0.001); accordingly, the time to diagnosis of NMO was shorter in the seronegative group (p < 0.029). The course of disease was more often monophasic in seronegatives (p < 0.008). Seropositives and seronegatives did not differ significantly with regard to age at onset, time to relapse, annualized relapse rates, outcome from relapse (complete, partial, no recovery), annualized EDSS increase, mortality rate, supratentorial brain lesions, brainstem lesions, history of carcinoma, frequency of preceding infections, oligoclonal bands, or CSF pleocytosis. Both the time to relapse and the time to diagnosis was longer if the disease started with ON (p < 0.002 and p < 0.013). Motor symptoms or tetraparesis at first myelitis and > 1 myelitis attacks in the first year were identified as possible predictors of a worse outcome."],["dc.identifier.doi","10.1186/1742-2094-9-14"],["dc.identifier.isi","000300949700001"],["dc.identifier.pmid","22260418"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7222"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27377"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1200"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Finck, Tobias L. K."],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.date.accessioned","2019-07-09T11:51:45Z"],["dc.date.available","2019-07-09T11:51:45Z"],["dc.date.issued","2019"],["dc.description.abstract","Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system (CNS), characterized by the infiltration of mononuclear cells into the CNS and a subsequent inflammation of the brain.Monocytes are implicated in disease pathogenesis not only in their function as potential antigen-presenting cells involved in the local reactivation of encephalitogenic T cells but also by independent effector functions contributing to structural damage and disease progression. However, monocytes also have beneficial effects as they can exert anti-inflammatory activity and promote tissue repair. Glucocorticoids (GCs) are widely used to treat acute relapses in MS patients. They act on a variety of cell types but their exact mechanisms of action including their modulation of monocyte function are not fully understood. Here we investigated effects of the therapeutically relevant GC methylprednisolone (MP) on monocytes from healthy individuals and MS patients in vitro and in vivo. The monocyte composition in the blood was different in MS patients compared to healthy individuals, but it was only marginally affected byMP treatment. In contrast, application ofMP caused amarked shift toward an anti-inflammatory monocyte phenotype in vitro and in vivo as revealed by an altered gene expression profile. Chemotaxis of monocytes toward CCL2, CCL5, and CX3CL1 was increased in MS patients compared to healthy individuals and further enhanced by MP pulse therapy. Both of these migration-promoting effects were more pronounced in MS patients with an acute relapse than in those with a progressive disease. Interestingly, the pro-migratory GC effect was independent of chemokine receptor levels as exemplified by results obtained for CCR2. Collectively, our findings suggest that GCs polarizemonocytes toward an anti-inflammatory phenotype and enhance their migration into the inflamed CNS, endowing them with the capacity to suppress the pathogenic immune response."],["dc.identifier.doi","10.3389/fimmu.2019.01200"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60002"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Glucocorticoid Therapy of Multiple Sclerosis Patients Induces Anti-inflammatory Polarization and Increased Chemotaxis of Monocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]