Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022779537> ?p ?o ?g. }
- W2022779537 endingPage "1683" @default.
- W2022779537 startingPage "1673" @default.
- W2022779537 abstract "Background— Inflammation has been closely linked to auto-immunogenic processes in atherosclerosis. Plasmacytoid dendritic cells (pDCs) are specialized to produce type-I interferons in response to pathogenic single-stranded nucleic acids, but can also sense self-DNA released from dying cells or in neutrophil extracellular traps complexed to the antimicrobial peptide Cramp/LL37 in autoimmune disease. However, the exact role of pDCs in atherosclerosis remains elusive. Methods and Results— Here we demonstrate that pDCs can be detected in murine and human atherosclerotic lesions. Exposure to oxidatively modified low-density lipoprotein enhanced the capacity of pDCs to phagocytose and prime antigen-specific T cell responses. Plasmacytoid DCs can be stimulated to produce interferon-α by Cramp/DNA complexes, and we further identified increased expression of Cramp and formation of neutrophil extracellular traps in atherosclerotic arteries. Whereas Cramp/DNA complexes aggravated atherosclerotic lesion formation in apolipoprotein E–deficient mice, pDC depletion and Cramp-deficiency in bone marrow reduced atherosclerosis and anti–double-stranded DNA antibody titers. Moreover, the specific activation of pDCs and interferon-α treatment promoted plaque growth, associated with enhanced anti–double-stranded–DNA antibody titers. Accordingly, anti–double-stranded DNA antibodies were elevated in patients with symptomatic versus asymptomatic carotid artery stenosis. Conclusions— Self-DNA (eg, released from dying cells or in neutrophil extracellular traps) and an increased expression of the antimicrobial peptide Cramp/LL37 in atherosclerotic lesions may thus stimulate a pDC-driven pathway of autoimmune activation and the generation of anti–double-stranded-DNA antibodies, critically aggravating atherosclerosis lesion formation. These key factors may thus represent novel therapeutic targets." @default.
- W2022779537 created "2016-06-24" @default.
- W2022779537 creator A5001883769 @default.
- W2022779537 creator A5004290451 @default.
- W2022779537 creator A5017294918 @default.
- W2022779537 creator A5017760830 @default.
- W2022779537 creator A5020472674 @default.
- W2022779537 creator A5028558012 @default.
- W2022779537 creator A5040698900 @default.
- W2022779537 creator A5049105192 @default.
- W2022779537 creator A5053337121 @default.
- W2022779537 creator A5062206583 @default.
- W2022779537 creator A5063726355 @default.
- W2022779537 creator A5063740703 @default.
- W2022779537 creator A5067597786 @default.
- W2022779537 creator A5069173292 @default.
- W2022779537 creator A5076904837 @default.
- W2022779537 creator A5089227561 @default.
- W2022779537 date "2012-04-03" @default.
- W2022779537 modified "2023-10-11" @default.
- W2022779537 title "Auto-Antigenic Protein-DNA Complexes Stimulate Plasmacytoid Dendritic Cells to Promote Atherosclerosis" @default.
- W2022779537 cites W154298887 @default.
- W2022779537 cites W175241905 @default.
- W2022779537 cites W1964147539 @default.
- W2022779537 cites W1964758221 @default.
- W2022779537 cites W1973431560 @default.
- W2022779537 cites W1975905715 @default.
- W2022779537 cites W1978741561 @default.
- W2022779537 cites W1980174384 @default.
- W2022779537 cites W1982130099 @default.
- W2022779537 cites W1993677761 @default.
- W2022779537 cites W2006738527 @default.
- W2022779537 cites W2008247360 @default.
- W2022779537 cites W2016486891 @default.
- W2022779537 cites W2017176563 @default.
- W2022779537 cites W2019916852 @default.
- W2022779537 cites W2020245957 @default.
- W2022779537 cites W2022273444 @default.
- W2022779537 cites W2029298122 @default.
- W2022779537 cites W2037435076 @default.
- W2022779537 cites W2049468976 @default.
- W2022779537 cites W2064371482 @default.
- W2022779537 cites W2066805794 @default.
- W2022779537 cites W2069227990 @default.
- W2022779537 cites W2084951281 @default.
- W2022779537 cites W2094901691 @default.
- W2022779537 cites W2096626379 @default.
- W2022779537 cites W2104934425 @default.
- W2022779537 cites W2117345276 @default.
- W2022779537 cites W2119252289 @default.
- W2022779537 cites W2123723916 @default.
- W2022779537 cites W2127222886 @default.
- W2022779537 cites W2133247340 @default.
- W2022779537 cites W2133779525 @default.
- W2022779537 cites W2134493657 @default.
- W2022779537 cites W2134595043 @default.
- W2022779537 cites W2136650071 @default.
- W2022779537 cites W2137540618 @default.
- W2022779537 cites W2138258126 @default.
- W2022779537 cites W2164596117 @default.
- W2022779537 cites W2166068186 @default.
- W2022779537 cites W2166635088 @default.
- W2022779537 cites W2168902918 @default.
- W2022779537 cites W2170866376 @default.
- W2022779537 cites W4252134514 @default.
- W2022779537 cites W4361866506 @default.
- W2022779537 cites W2098751820 @default.
- W2022779537 doi "https://doi.org/10.1161/circulationaha.111.046755" @default.
- W2022779537 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22388324" @default.
- W2022779537 hasPublicationYear "2012" @default.
- W2022779537 type Work @default.
- W2022779537 sameAs 2022779537 @default.
- W2022779537 citedByCount "298" @default.
- W2022779537 countsByYear W20227795372012 @default.
- W2022779537 countsByYear W20227795372013 @default.
- W2022779537 countsByYear W20227795372014 @default.
- W2022779537 countsByYear W20227795372015 @default.
- W2022779537 countsByYear W20227795372016 @default.
- W2022779537 countsByYear W20227795372017 @default.
- W2022779537 countsByYear W20227795372018 @default.
- W2022779537 countsByYear W20227795372019 @default.
- W2022779537 countsByYear W20227795372020 @default.
- W2022779537 countsByYear W20227795372021 @default.
- W2022779537 countsByYear W20227795372022 @default.
- W2022779537 countsByYear W20227795372023 @default.
- W2022779537 crossrefType "journal-article" @default.
- W2022779537 hasAuthorship W2022779537A5001883769 @default.
- W2022779537 hasAuthorship W2022779537A5004290451 @default.
- W2022779537 hasAuthorship W2022779537A5017294918 @default.
- W2022779537 hasAuthorship W2022779537A5017760830 @default.
- W2022779537 hasAuthorship W2022779537A5020472674 @default.
- W2022779537 hasAuthorship W2022779537A5028558012 @default.
- W2022779537 hasAuthorship W2022779537A5040698900 @default.
- W2022779537 hasAuthorship W2022779537A5049105192 @default.
- W2022779537 hasAuthorship W2022779537A5053337121 @default.
- W2022779537 hasAuthorship W2022779537A5062206583 @default.
- W2022779537 hasAuthorship W2022779537A5063726355 @default.
- W2022779537 hasAuthorship W2022779537A5063740703 @default.