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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.accessioned2017-03-14T11:41:34Z
dc.date.available2017-03-14T11:41:34Z
dc.date.issued2016-08-31
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.en_US
dc.descriptionSource: <a href=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5166441/>doi: 10.1189/jlb.3VMR0316-132R</a>en_US
dc.identifier.citationBarratt-Due A, Pischke SE, Nilsson P, Espevik T, Mollnes TE. Dual inhibition of complement and Toll-like receptors as a novel approach to treat inflammatory diseases-C3 or C5 emerge together with CD14 as promising targets.. Journal of Leukocyte Biology. 2016en_US
dc.identifier.cristinIDFRIDAID 1439419
dc.identifier.doi10.1189/jlb.3VMR0316-132R
dc.identifier.issn0741-5400
dc.identifier.issn1938-3673
dc.identifier.urihttps://hdl.handle.net/10037/10644
dc.language.isoengen_US
dc.publisherSociety for Leukocyte Biology. Journal of Leukocyte Biologyen_US
dc.relation.journalJournal of Leukocyte Biology
dc.relation.projectIDStiftelsen Kristian Gerhard Jebsen: SKGJ-MED-012en_US
dc.relation.projectIDNorges forskningsråd: 223255en_US
dc.rights.accessRightsopenAccessen_US
dc.subjectVDP::Medisinske Fag: 700en_US
dc.subjectinnate immunityen_US
dc.subjectinflammationen_US
dc.subjecttherapyen_US
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 targets.en_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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