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Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-5779
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dc.contributor.authorHauptmann, Judith-
dc.contributor.authorJohann, Lisa-
dc.contributor.authorMarini, Federico-
dc.contributor.authorKitic, Maja-
dc.contributor.authorColombo, Elisa-
dc.contributor.authorMufazalov, Ilgiz A.-
dc.contributor.authorKrueger, Martin-
dc.contributor.authorKarram, Khalad-
dc.contributor.authorMoos, Sonja-
dc.contributor.authorWanke, Florian-
dc.contributor.authorKurschus, Florian C.-
dc.contributor.authorKlein, Matthias-
dc.contributor.authorCardoso, Silvia-
dc.contributor.authorStrauß, Judith-
dc.contributor.authorBolisetty, Subhashini-
dc.contributor.authorLühder, Fred-
dc.contributor.authorSchwaninger, Markus-
dc.contributor.authorBinder, Harald-
dc.contributor.authorBechman, Ingo-
dc.contributor.authorBopp, Tobias-
dc.contributor.authorAgarwal, Anupam-
dc.contributor.authorSoares, Miguel P.-
dc.contributor.authorRegen, Tommy-
dc.contributor.authorWaisman, Ari-
dc.date.accessioned2021-05-07T08:20:19Z-
dc.date.available2021-05-07T08:20:19Z-
dc.date.issued2020-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/5788-
dc.description.abstractThe proinflammatory cytokine interleukin 1 (IL-1) is crucially involved in the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Herein, we studied the role of IL-1 signaling in blood–brain barrier (BBB) endothelial cells (ECs), astrocytes and microglia for EAE development, using mice with the conditional deletion of its signaling receptor IL-1R1. We found that IL-1 signaling in microglia and astrocytes is redundant for the development of EAE, whereas the IL-1R1 deletion in BBB-ECs markedly ameliorated disease severity. IL-1 signaling in BBB-ECs upregulated the expression of the adhesion molecules Vcam-1, Icam-1 and the chemokine receptor Darc, all of which have been previously shown to promote CNS-specific inflammation. In contrast, IL-1R1 signaling suppressed the expression of the stress-responsive heme catabolizing enzyme heme oxygenase-1 (HO-1) in BBB-ECs, promoting disease progression via a mechanism associated with deregulated expression of the IL-1-responsive genes Vcam1, Icam1 and Ackr1 (Darc). Mechanistically, our data emphasize a functional crosstalk of BBB-EC IL-1 signaling and HO-1, controlling the transcription of downstream proinflammatory genes promoting the pathogenesis of autoimmune neuroinflammation.en_GB
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleInterleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood–brain barrieren_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-5779-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleActa neuropathologicade
jgu.journal.volume140de
jgu.pages.start549de
jgu.pages.end567de
jgu.publisher.year2020-
jgu.publisher.nameSpringerde
jgu.publisher.placeBerlin u.a.de
jgu.publisher.urihttps://doi.org/10.1007/s00401-020-02187-xde
jgu.publisher.issn1432-0533de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1007/s00401-020-02187-x
jgu.organisation.rorhttps://ror.org/023b0x485
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