Vis enkel innførsel

dc.contributor.authorBarratt-Due, Andreas
dc.contributor.authorPischke, Søren Erik
dc.contributor.authorNilsson, Per
dc.contributor.authorEspevik, Terje
dc.contributor.authorMollnes, Tom Eirik
dc.date.accessioned2017-10-31T08:03:23Z
dc.date.available2017-10-31T08:03:23Z
dc.date.created2017-01-27T14:05:03Z
dc.date.issued2016
dc.identifier.citationJournal of Leukocyte Biology. 2016, .nb_NO
dc.identifier.issn0741-5400
dc.identifier.urihttp://hdl.handle.net/11250/2463029
dc.description.abstractThe host is protected by pattern recognition systems, including complement and TLRs, which are closely cross-talking. If improperly activated, these systems might induce tissue damage and disease. Inhibition of single downstream proinflammatory cytokines, such as TNF, IL-1β, and IL-6, have failed in clinical sepsis trials, which might not be unexpected, given the substantial amounts of mediators involved in the pathogenesis of this condition. Instead, we have put forward a hypothesis of inhibition at the recognition phase by “dual blockade” of bottleneck molecules of complement and TLRs. By acting upstream and broadly, the dual blockade could be beneficial in conditions with improper or uncontrolled innate immune activation threatening the host. Key bottleneck molecules in these systems that could be targets for inhibition are the central complement molecules C3 and C5 and the important CD14 molecule, which is a coreceptor for several TLRs, including TLR4 and TLR2. This review summarizes current knowledge of inhibition of complement and TLRs alone and in combination, in both sterile and nonsterile inflammatory processes, where activation of these systems is of crucial importance for tissue damage and disease. Thus, dual blockade might provide a general, broad-acting therapeutic regimen against a number of diseases where innate immunity is improperly activated.nb_NO
dc.language.isoengnb_NO
dc.publisherSociety for Leukocyte Biologynb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleDual inhibition of complement and Toll-like receptors as a novel approach to treat inflammatory diseases-C3 or C5 emerge together with CD14 as promising targetsnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.pagenumber13nb_NO
dc.source.journalJournal of Leukocyte Biologynb_NO
dc.identifier.doi10.1189/jlb.3VMR0316-132R
dc.identifier.cristin1439419
dc.relation.projectStiftelsen Kristian Gerhard Jebsen: SKGJ-MED-012nb_NO
dc.relation.projectNorges forskningsråd: 223255nb_NO
dc.description.localcode© The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International (CC BY 4.0) (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.nb_NO
cristin.unitcode194,65,15,30
cristin.unitcode194,65,15,0
cristin.unitnameCentre of Molecular Inflammation Research (SFF-CEMIR)
cristin.unitnameInstitutt for kreftforskning og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


Tilhørende fil(er)

Thumbnail

Denne innførselen finnes i følgende samling(er)

Vis enkel innførsel

Navngivelse 4.0 Internasjonal
Med mindre annet er angitt, så er denne innførselen lisensiert som Navngivelse 4.0 Internasjonal