FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2190977173> ?p ?o ?g. }

• W2190977173 endingPage "e1005673" @default.
• W2190977173 startingPage "e1005673" @default.
• W2190977173 abstract "Human β-defensin 3 (hBD3) is a cationic host defence peptide and is part of the innate immune response. HBD3 is present on a highly copy number variable block of six β-defensin genes, and increased copy number is associated with the autoimmune disease psoriasis. It is not known how this increase influences disease development, but psoriasis is a T cell-mediated disease and activation of the innate immune system is required for the initial trigger that leads to the amplification stage. We investigated the effect of hBD3 on the response of primary macrophages to various TLR agonists. HBD3 exacerbated the production of type I Interferon-β in response to the viral ligand mimic polyinosinic:polycytidylic acid (polyI:C) in both human and mouse primary cells, although production of the chemokine CXCL10 was suppressed. Compared to polyI:C alone, mice injected with both hBD3 peptide and polyI:C also showed an enhanced increase in Interferon-β. Mice expressing a transgene encoding hBD3 had elevated basal levels of Interferon-β, and challenge with polyI:C further increased this response. HBD3 peptide increased uptake of polyI:C by macrophages, however the cellular response and localisation of polyI:C in cells treated contemporaneously with hBD3 or cationic liposome differed. Immunohistochemistry showed that hBD3 and polyI:C do not co-localise, but in the presence of hBD3 less polyI:C localises to the early endosome. Using bone marrow derived macrophages from knockout mice we demonstrate that hBD3 suppresses the polyI:C-induced TLR3 response mediated by TICAM1 (TRIF), while exacerbating the cytoplasmic response through MDA5 (IFIH1) and MAVS (IPS1/CARDIF). Thus, hBD3, a highly copy number variable gene in human, influences cellular responses to the viral mimic polyI:C implying that copy number may have a significant phenotypic effect on the response to viral infection and development of autoimmunity in humans." @default.
• W2190977173 created "2016-06-24" @default.
• W2190977173 creator A5010363328 @default.
• W2190977173 creator A5034744149 @default.
• W2190977173 creator A5053241806 @default.
• W2190977173 creator A5071147820 @default.
• W2190977173 creator A5075090993 @default.
• W2190977173 creator A5075994602 @default.
• W2190977173 creator A5079192220 @default.
• W2190977173 creator A5081490392 @default.
• W2190977173 creator A5082513087 @default.
• W2190977173 creator A5087913881 @default.
• W2190977173 creator A5088710728 @default.
• W2190977173 creator A5088847857 @default.
• W2190977173 date "2015-12-08" @default.
• W2190977173 modified "2023-10-14" @default.
• W2190977173 title "Human β-D-3 Exacerbates MDA5 but Suppresses TLR3 Responses to the Viral Molecular Pattern Mimic Polyinosinic:Polycytidylic Acid" @default.
• W2190977173 cites W1527143867 @default.
• W2190977173 cites W1571292455 @default.
• W2190977173 cites W1583708762 @default.
• W2190977173 cites W1585125753 @default.
• W2190977173 cites W1720483047 @default.
• W2190977173 cites W1761972135 @default.
• W2190977173 cites W1841739835 @default.
• W2190977173 cites W1966621175 @default.
• W2190977173 cites W1972599527 @default.
• W2190977173 cites W1979404035 @default.
• W2190977173 cites W1979749047 @default.
• W2190977173 cites W1989656760 @default.
• W2190977173 cites W1999534520 @default.
• W2190977173 cites W2000023558 @default.
• W2190977173 cites W2000871561 @default.
• W2190977173 cites W2008580692 @default.
• W2190977173 cites W2010191716 @default.
• W2190977173 cites W2018308755 @default.
• W2190977173 cites W2020040634 @default.
• W2190977173 cites W2020173029 @default.
• W2190977173 cites W2022675876 @default.
• W2190977173 cites W2028575270 @default.
• W2190977173 cites W2039854579 @default.
• W2190977173 cites W2054065543 @default.
• W2190977173 cites W2060351820 @default.
• W2190977173 cites W2061974718 @default.
• W2190977173 cites W2063310200 @default.
• W2190977173 cites W2065554630 @default.
• W2190977173 cites W2069096108 @default.
• W2190977173 cites W2070740895 @default.
• W2190977173 cites W2084175456 @default.
• W2190977173 cites W2098225479 @default.
• W2190977173 cites W2100446659 @default.
• W2190977173 cites W2101567516 @default.
• W2190977173 cites W2102889851 @default.
• W2190977173 cites W2116942392 @default.
• W2190977173 cites W2117440442 @default.
• W2190977173 cites W2124733101 @default.
• W2190977173 cites W2125566625 @default.
• W2190977173 cites W2127096990 @default.
• W2190977173 cites W2137357450 @default.
• W2190977173 cites W2138006624 @default.
• W2190977173 cites W2140815975 @default.
• W2190977173 cites W2169758620 @default.
• W2190977173 cites W4249486154 @default.
• W2190977173 doi "https://doi.org/10.1371/journal.pgen.1005673" @default.
• W2190977173 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4672878" @default.
• W2190977173 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26646717" @default.
• W2190977173 hasPublicationYear "2015" @default.
• W2190977173 type Work @default.
• W2190977173 sameAs 2190977173 @default.
• W2190977173 citedByCount "20" @default.
• W2190977173 countsByYear W21909771732016 @default.
• W2190977173 countsByYear W21909771732017 @default.
• W2190977173 countsByYear W21909771732018 @default.
• W2190977173 countsByYear W21909771732019 @default.
• W2190977173 countsByYear W21909771732020 @default.
• W2190977173 countsByYear W21909771732021 @default.
• W2190977173 countsByYear W21909771732022 @default.
• W2190977173 countsByYear W21909771732023 @default.
• W2190977173 crossrefType "journal-article" @default.
• W2190977173 hasAuthorship W2190977173A5010363328 @default.
• W2190977173 hasAuthorship W2190977173A5034744149 @default.
• W2190977173 hasAuthorship W2190977173A5053241806 @default.
• W2190977173 hasAuthorship W2190977173A5071147820 @default.
• W2190977173 hasAuthorship W2190977173A5075090993 @default.
• W2190977173 hasAuthorship W2190977173A5075994602 @default.
• W2190977173 hasAuthorship W2190977173A5079192220 @default.
• W2190977173 hasAuthorship W2190977173A5081490392 @default.
• W2190977173 hasAuthorship W2190977173A5082513087 @default.
• W2190977173 hasAuthorship W2190977173A5087913881 @default.
• W2190977173 hasAuthorship W2190977173A5088710728 @default.
• W2190977173 hasAuthorship W2190977173A5088847857 @default.
• W2190977173 hasBestOaLocation W21909771731 @default.
• W2190977173 hasConcept C104317684 @default.
• W2190977173 hasConcept C13373296 @default.
• W2190977173 hasConcept C134474686 @default.
• W2190977173 hasConcept C136449434 @default.
• W2190977173 hasConcept C153911025 @default.
• W2190977173 hasConcept C166703698 @default.
• W2190977173 hasConcept C203014093 @default.

• next