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dc.contributor.authorHovland, Anders
dc.contributor.authorJonasson, Lena
dc.contributor.authorGarred, Peter
dc.contributor.authorYndestad, Arne
dc.contributor.authorAukrust, Pål
dc.contributor.authorLappegård, Knut Tore
dc.contributor.authorEspevik, Terje
dc.contributor.authorMollnes, Tom Eirik
dc.identifier.citationAtherosclerosis 2015, 241(2):480-494nb_NO
dc.description.abstractDespite recent medical advances, atherosclerosis is a global burden accounting for numerous deaths and hospital admissions. Immune-mediated inflammation is a major component of the atherosclerotic process, but earlier research focus on adaptive immunity has gradually switched towards the role of innate immunity. The complement system and toll-like receptors (TLRs), and the crosstalk between them, may be of particular interest both with respect to pathogenesis and as therapeutic targets in atherosclerosis. Animal studies indicate that inhibition of C3a and C5a reduces atherosclerosis. In humans modified LDL-cholesterol activate complement and TLRs leading to downstream inflammation, and histopathological studies indicate that the innate immune system is present in atherosclerotic lesions. Moreover, clinical studies have demonstrated that both complement and TLRs are upregulated in atherosclerotic diseases, although interventional trials have this far been disappointing. However, based on recent research showing an intimate interplay between complement and TLRs we propose a model in which combined inhibition of both complement and TLRs may represent a potent anti-inflammatory therapeutic approach to reduce atherosclerosis.nb_NO
dc.titleThe complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosisnb_NO
dc.typePeer reviewednb_NO
dc.typeJournal articleen_GB
dc.relation.projectNorges forskningsråd: 223255nb_NO
dc.description.localcodeAttribution-NonCommercial-NoDerivatives 4.0 Internationalnb_NO

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