Hanisch, Uwe-Karsten

[["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.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Nitsche, M."],["dc.contributor.author","Mekler, D."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Heikenwalder, Mathias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T10:58:20Z"],["dc.date.available","2018-11-07T10:58:20Z"],["dc.date.issued","2007"],["dc.format.extent","S255"],["dc.identifier.isi","000251423400794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50454"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","23rd Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis/12th Annual Conference of Rehabilitation in MS"],["dc.relation.eventlocation","Prague, CZECH REPUBLIC"],["dc.relation.issn","1352-4585"],["dc.title","Microglia in the adult brain arise from Ly-6Chi monocytes only under defined host conditions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4841"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","4848"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Hermann, Isabel"],["dc.contributor.author","Kellert, Markus"],["dc.contributor.author","Schmidt, Hauke"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T09:28:40Z"],["dc.date.available","2018-11-07T09:28:40Z"],["dc.date.issued","2006"],["dc.description.abstract","The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG(35-55)) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG(35-55) injection but was more severe in animals infected 7 days after the first MOG(35-55) injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier."],["dc.identifier.doi","10.1128/IAI.00026-06"],["dc.identifier.isi","000239381400049"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30836"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Streptococcus pneumoniae infection aggravates experimental autoimmune encephalomyelitis via toll-like receptor 2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cytokine"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Rossum van, Denise"],["dc.contributor.author","Weinstein, Jonathan R."],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Moeller, Thomas"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T11:11:15Z"],["dc.date.available","2018-11-07T11:11:15Z"],["dc.date.issued","2008"],["dc.format.extent","315"],["dc.identifier.doi","10.1016/j.cyto.2008.07.386"],["dc.identifier.isi","000260212900351"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53386"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd Elsevier Science Ltd"],["dc.publisher.place","London"],["dc.relation.conference","7th Joint Conference of the International-Cytokine-Society/International-Society-for-Interferon-and- Cytoklin-Research"],["dc.relation.eventlocation","Montreal, CANADA"],["dc.relation.issn","1043-4666"],["dc.title","Toll-like receptor 4/MyD88 pathway mediates microglial proinflammatory cytokine responses to thrombin-associated coagulation protein complexes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","153"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","178"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Schmidt, Hauke"],["dc.contributor.author","Detje, Claudia N."],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Becher, Burkhard"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Kalinke, Ulrich"],["dc.date.accessioned","2018-11-07T09:21:15Z"],["dc.date.available","2018-11-07T09:21:15Z"],["dc.date.issued","2006"],["dc.identifier.isi","000241633101059"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29069"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","8th International Conference of Neuroimmunology"],["dc.relation.eventlocation","Nagoya, JAPAN"],["dc.relation.issn","0165-5728"],["dc.title","Type 1 interferon receptor (IFNAR)-dependent modulation of myeloid cell activation determines the course of 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.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Nitsche, M."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Hanisch, U-K"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Heikenwalder, Mathias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T10:58:41Z"],["dc.date.available","2018-11-07T10:58:41Z"],["dc.date.issued","2007"],["dc.format.extent","320"],["dc.identifier.isi","000249149200058"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50522"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","Joint Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy (DGNN)/Polish-Associatin-of-Neuropathologists"],["dc.relation.eventlocation","Greifswald, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Microglia in the adult brain arise from Ly-6 Chi monocytes only under defined host conditions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Detje, Claudia N."],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Knobeloch, K."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Becher, Burkhard"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Kalinke, Ulrich"],["dc.date.accessioned","2018-11-07T09:22:53Z"],["dc.date.available","2018-11-07T09:22:53Z"],["dc.date.issued","2006"],["dc.format.extent","S52"],["dc.identifier.isi","000241921400168"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29446"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","22nd Congress of the European-Committee-for-the-Treatment-and-Resarch-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","1352-4585"],["dc.title","Type 1 interferon receptor (IFNAR)-dependent modulation of myeloid cell activation determines the course of 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.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Kalinke, Ulrich"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T10:55:51Z"],["dc.date.available","2018-11-07T10:55:51Z"],["dc.date.issued","2005"],["dc.format.extent","340"],["dc.identifier.isi","000232160500092"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49881"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","50th Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Graz, AUSTRIA"],["dc.relation.issn","0001-6322"],["dc.title","Lack of Type 1 Interferon Receptor (IFNAR) leads to exacerbation of 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.journal","Glia"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Kastriti, Maria-Eleni"],["dc.contributor.author","Revelo, Natalia H."],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Borisch, Angela"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T08:51:34Z"],["dc.date.available","2018-11-07T08:51:34Z"],["dc.date.issued","2011"],["dc.format.extent","S148"],["dc.identifier.isi","000294178900582"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21965"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.issn","0894-1491"],["dc.title","CD14 AND TRIF GOVERN DISTINCT RESPONSIVENESS AND RESPONSES IN MOUSE MICROGLIAL TLR4 CHALLENGES BY STRUCTURAL VARIANTS OF LPS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1544"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","1553"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, Hauke"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Heikenwalder, Mathias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T10:49:48Z"],["dc.date.available","2018-11-07T10:49:48Z"],["dc.date.issued","2007"],["dc.description.abstract","Microglia are crucially important myeloid cells in the CNS and constitute the first immunological barrier against pathogens and environmental insults. The factors controlling microglia recruitment from the blood remain elusive and the direct circulating microglia precursor has not yet been identified in vivo. Using a panel of bone marrow chimeric and adoptive transfer experiments, we found that circulating Ly-6C(hi)CCR2(+) monocytes were preferentially recruited to the lesioned brain and differentiated into microglia. Notably, microglia engraftment in CNS pathologies, which are not associated with overt blood-brain barrier disruption, required previous conditioning of brain (for example, by direct tissue irradiation). Our results identify Ly-6C(hi)CCR2(+) monocytes as direct precursors of microglia in the adult brain and establish the importance of local factors in the adult CNS for microglia engraftment."],["dc.identifier.doi","10.1038/nn2015"],["dc.identifier.isi","000251172900011"],["dc.identifier.pmid","18026096"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48513"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1097-6256"],["dc.title","Microglia in the adult brain arise from Ly-6C(hi)CCR2(+) monocytes only under defined host conditions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]