Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-760
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dc.contributor.authorBent, Rebekka-
dc.contributor.authorMoll, Lorna-
dc.contributor.authorGrabbe, Stephan-
dc.contributor.authorBros, Matthias-
dc.date.accessioned2018-11-26T14:57:50Z-
dc.date.available2018-11-26T15:57:50Z-
dc.date.issued2018-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/762-
dc.description.abstractInterleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL-1β expression and its multi-facetted role in pathophysiological conditions. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4+ T cells towards T helper type (Th) 1 and Th17 cells. Therefore, IL-1β has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1β generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1β generated within the tumor microenvironment predominantly by tumor-infiltrating macrophages promotes tumor growth and metastasis via different mechanisms. These include the expression of IL-1 targets which promote neoangiogenesis and of soluble mediators in cancer-associated fibroblasts that evoke antiapoptotic signaling in tumor cells. Moreover, IL-1 promotes the propagation of myeloid-derived suppressor cells. Using genetic mouse models as well as agents for pharmacological inhibition of IL-1 signaling therapeutically applied for treatment of IL-1 associated autoimmune diseases indicate that IL-1β is a driver of tumor induction and development.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin-
dc.language.isoeng-
dc.rightsCC BYde_DE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleInterleukin-1 beta - a friend or foe in malignancies?en_GB
dc.typeZeitschriftenaufsatzde_DE
dc.identifier.urnurn:nbn:de:hebis:77-publ-586594-
dc.identifier.doihttp://doi.org/10.25358/openscience-760-
jgu.type.dinitypearticle-
jgu.type.versionPublished versionen_GB
jgu.type.resourceText-
jgu.organisation.departmentFB 04 Medizin-
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleInternational journal of molecular sciences-
jgu.journal.volume19-
jgu.journal.issue8-
jgu.pages.alternativeArt. 2155-
jgu.publisher.year2018-
jgu.publisher.nameMolecular Diversity Preservation International-
jgu.publisher.placeBasel-
jgu.publisher.urihttp://dx.doi.org/10.3390/ijms19082155-
jgu.publisher.issn1422-0067-
jgu.publisher.issn1661-6596-
jgu.organisation.placeMainz-
jgu.subject.ddccode610-
opus.date.accessioned2018-11-26T14:57:50Z-
opus.date.modified2018-11-28T09:40:26Z-
opus.date.available2018-11-26T15:57:50-
opus.subject.dfgcode00-000-
opus.organisation.stringFB 04: Medizin: Hautklinikde_DE
opus.identifier.opusid58659-
opus.institute.number0431-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_GB
opus.affiliatedGrabbe, Stephan-
opus.affiliatedBros, Matthias-
jgu.publisher.doi10.3390/ijms19082155
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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