Please use this identifier to cite or link to this item:
http://doi.org/10.25358/openscience-760
Full metadata record
DC Field | Value | Language |
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dc.contributor.author | Bent, Rebekka | - |
dc.contributor.author | Moll, Lorna | - |
dc.contributor.author | Grabbe, Stephan | - |
dc.contributor.author | Bros, Matthias | - |
dc.date.accessioned | 2018-11-26T14:57:50Z | - |
dc.date.available | 2018-11-26T15:57:50Z | - |
dc.date.issued | 2018 | - |
dc.identifier.uri | https://openscience.ub.uni-mainz.de/handle/20.500.12030/762 | - |
dc.description.abstract | Interleukin-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.sponsorship | DFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin | - |
dc.language.iso | eng | - |
dc.rights | CC BY | de_DE |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | - |
dc.subject.ddc | 610 Medizin | de_DE |
dc.subject.ddc | 610 Medical sciences | en_GB |
dc.title | Interleukin-1 beta - a friend or foe in malignancies? | en_GB |
dc.type | Zeitschriftenaufsatz | de_DE |
dc.identifier.urn | urn:nbn:de:hebis:77-publ-586594 | - |
dc.identifier.doi | http://doi.org/10.25358/openscience-760 | - |
jgu.type.dinitype | article | - |
jgu.type.version | Published version | en_GB |
jgu.type.resource | Text | - |
jgu.organisation.department | FB 04 Medizin | - |
jgu.organisation.number | 2700 | - |
jgu.organisation.name | Johannes Gutenberg-Universität Mainz | - |
jgu.rights.accessrights | openAccess | - |
jgu.journal.title | International journal of molecular sciences | - |
jgu.journal.volume | 19 | - |
jgu.journal.issue | 8 | - |
jgu.pages.alternative | Art. 2155 | - |
jgu.publisher.year | 2018 | - |
jgu.publisher.name | Molecular Diversity Preservation International | - |
jgu.publisher.place | Basel | - |
jgu.publisher.uri | http://dx.doi.org/10.3390/ijms19082155 | - |
jgu.publisher.issn | 1422-0067 | - |
jgu.publisher.issn | 1661-6596 | - |
jgu.organisation.place | Mainz | - |
jgu.subject.ddccode | 610 | - |
opus.date.accessioned | 2018-11-26T14:57:50Z | - |
opus.date.modified | 2018-11-28T09:40:26Z | - |
opus.date.available | 2018-11-26T15:57:50 | - |
opus.subject.dfgcode | 00-000 | - |
opus.organisation.string | FB 04: Medizin: Hautklinik | de_DE |
opus.identifier.opusid | 58659 | - |
opus.institute.number | 0431 | - |
opus.metadataonly | false | - |
opus.type.contenttype | Keine | de_DE |
opus.type.contenttype | None | en_GB |
opus.affiliated | Grabbe, Stephan | - |
opus.affiliated | Bros, Matthias | - |
jgu.publisher.doi | 10.3390/ijms19082155 | |
jgu.organisation.ror | https://ror.org/023b0x485 | |
Appears in collections: | JGU-Publikationen |