http://purl.uniprot.org/citations/23152543 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/23152543 | http://www.w3.org/2000/01/rdf-schema#comment | "Persistent high fever is one of the most typical clinical symptoms in dengue virus (DV)-infected patients. However, the source of endogenous pyrogen (eg, IL-1β) and the signaling cascade leading to the activation of inflammasome and caspase-1, which are essential for IL-1β and IL-18 secretion, during dengue infection have not been elucidated yet. Macrophages can be polarized into distinct phenotypes under the influence of GM-CSF or M-CSF, denoted as GM-Mϕ and M-Mϕ, respectively. We found that DV induced high levels of IL-1β and IL-18 from GM-Mϕ (inflammatory macrophage) and caused cell death (pyroptosis), whereas M-Mϕ (resting macrophage) did not produce IL-1β and IL-18 on DV infection even with lipopolysaccharide priming. This observation demonstrates the distinct responses of GM-Mϕ and M-Mϕ to DV infection. Moreover, up-regulation of pro-IL-1β, pro-IL-18, and NLRP3 associated with caspase-1 activation was observed in DV-infected GM-Mϕ, whereas blockade of CLEC5A/MDL-1, a C-type lectin critical for dengue hemorrhagic fever and Japanese encephalitis virus infection, inhibits NLRP3 inflammasome activation and pyrotopsis in GM-Mϕ. Thus, DV can activate NLRP3 inflammasome via CLEC5A, and GM-Mϕ plays a more important role than M-Mϕ in the pathogenesis of DV infection."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2012-05-430090"xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Hsieh S.L."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Li L."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Wu M.F."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Chen S.T."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Lin Y.L."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Lin W.W."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Yang A.H."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Chen N.J."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/author | "Tsai I.S."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/pages | "95-106"xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/title | "CLEC5A is critical for dengue virus-induced inflammasome activation in human macrophages."xsd:string |
http://purl.uniprot.org/citations/23152543 | http://purl.uniprot.org/core/volume | "121"xsd:string |
http://purl.uniprot.org/citations/23152543 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23152543 |
http://purl.uniprot.org/citations/23152543 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23152543 |
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http://purl.uniprot.org/uniprot/Q9NY25 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/23152543 |