title: Expression of toll-like receptors in human atherosclerotic lesions: a possible pathway for plaque activation.
abstract: BACKGROUND
  Innate immune reactions against bacteria and viruses have been implicated in the pathogenesis of atherosclerosis. To explore the molecular mechanism by which microbe recognition occurs in the artery wall, we characterized the expression of toll-like receptors (TLRs), a family of pathogen pattern recognition receptors, in atherosclerotic lesions.
  
  
  RESULTS
  Semiquantitative polymerase chain reaction and immunohistochemical analysis demonstrated that of 9 TLRs, the expression of TLR1, TLR2, and TLR4 was markedly enhanced in human atherosclerotic plaques. A considerable proportion of TLR-expressing cells were also activated, as shown by the nuclear translocation of nuclear factor-kappaB.
  
  
  CONCLUSIONS
  Our findings illustrate a repertoire of TLRs associated with inflammatory activation in human atherosclerotic lesions, and they encourage further exploration of innate immunity in the pathogenesis of atherosclerosis.
authors.affiliation: Center for Molecular Medicine and the Department of Medicine, Karolinska Institute, Stockholm, Sweden.
authors.forename: Kristina
authors.initials: K
authors.lastname: Edfeldt
authors.forename: Jesper
authors.initials: J
authors.lastname: Swedenborg
authors.forename: Göran K
authors.initials: GK
authors.lastname: Hansson
authors.forename: Zhong-qun
authors.initials: ZQ
authors.lastname: Yan
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D001161:Arteriosclerosis / Q000378:metabolism* / Q000473:pathology; D015415:Biomarkers / Q000032:analysis; D017252:CD3 Complex / Q000096:biosynthesis; D016893:Carotid Stenosis / Q000378:metabolism / Q000473:pathology; D029721:Drosophila Proteins; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008323:Mammary Arteries / Q000378:metabolism / Q000473:pathology; D008562:Membrane Glycoproteins / Q000096:biosynthesis* / Q000235:genetics; D016328:NF-kappa B / Q000096:biosynthesis; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D011956:Receptors, Cell Surface / Q000096:biosynthesis* / Q000235:genetics; D051194:Toll-Like Receptor 1; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D051996:Transcription Factor RelA; D014841:von Willebrand Factor / Q000096:biosynthesis; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D017252:CD3 Complex; D029721:Drosophila Proteins; D008562:Membrane Glycoproteins; D016328:NF-kappa B; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D051194:Toll-Like Receptor 1; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D051996:Transcription Factor RelA; D014841:von Willebrand Factor; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C495342:TLR2 protein, human; C495345:TLR4 protein, human