About: Pivotal Advance: The promotion of soluble DC‐SIGN release by inflammatory signals and its enhancement of cytomegalovirus‐mediated cis‐infection of myeloid dendritic cells

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About: Pivotal Advance: The promotion of soluble DC‐SIGN release by inflammatory signals and its enhancement of cytomegalovirus‐mediated cis‐infection of myeloid dendritic cells Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Pivotal Advance: The promotion of soluble DC‐SIGN release by inflammatory signals and its enhancement of cytomegalovirus‐mediated cis‐infection of myeloid dendritic cells
Creator	Halary, F Hocke, C Humbert, J.-M Plazolles, N Vachot, L Verrier, B
Source	PMC
abstract	DC‐SIGN is a member of the C‐type lectin family. Mainly expressed by myeloid DCs, it is involved in the capture and internalization of pathogens, including human CMV. Several transcripts have been identified, some of which code for putative soluble proteins. However, little is known about the regulation and the functional properties of such putative sDC‐SIGN variants. To better understand how sDC‐SIGN could be involved in CMV infection, we set out to characterize biochemical and functional properties of rDC‐SIGN as well as naturally occurring sDC‐SIGN. We first developed a specific, quantitative ELISA and then used it to detect the presence sDC‐SIGN in in vitro‐generated DC culture supernatants as cell‐free secreted tetramers. Next, in correlation with their inflammatory status, we demonstrated the presence of sDC‐SIGN in several human body fluids, including serum, joint fluids, and BALs. CMV infection of human tissues was also shown to promote sDC‐SIGN release. Based on the analysis of the cytokine/chemokine content of sDC‐SIGN culture supernatants, we identified IFN‐γ and CXCL8/IL‐8 as inducers of sDC‐SIGN production by MoDC. Finally, we demonstrated that sDC‐SIGN was able to interact with CMV gB under native conditions, leading to a significant increase in MoDC CMV infection. Overall, our results confirm that sDC‐SIGN, like its well‐known, counterpart mDC‐SIGN, may play a pivotal role in CMV‐mediated pathogenesis.
has issue date	2010-10-12(xsd:dateTime)
bibo:doi	10.1189/jlb.0710386
bibo:pmid	20940323
has license	no-cc
sha1sum (hex)	3eaa51a10f379eab54bc320342f511459344a065
schema:url	https://doi.org/10.1189/jlb.0710386
resource representing a document's title	Pivotal Advance: The promotion of soluble DC‐SIGN release by inflammatory signals and its enhancement of cytomegalovirus‐mediated cis‐infection of myeloid dendritic cells
has PubMed Central identifier	PMC7166666
has PubMed identifier	20940323
schema:publication	J Leukoc Biol
resource representing a document's body	covid:3eaa51a10f379eab54bc320342f511459344a065#body_text
is schema:about of	named entity 'correlation' named entity 'human body' named entity 'code' named entity 'biochemical' named entity 'INCLUDING' named entity 'FLUIDS' named entity 'CAPTURE' named entity 'TO CHARACTERIZE' named entity 'PROTEINS' named entity 'NATIVE' named entity 'MDC' named entity 'PROMOTE' named entity 'TO DETECT' named entity 'TO INTERACT WITH' named entity 'RDC' named entity 'OVERALL' named entity 'KNOWN' named entity 'ROLE' named entity 'SOLUBLE' named entity 'expressed' named entity 'DCs' named entity 'CMV' named entity 'human tissues' named entity 'set' named entity 'infection' named entity 'native' named entity 'leading' named entity 'soluble' named entity 'body fluids' named entity 'enhancement' named entity 'myeloid dendritic cells' named entity 'DCs' named entity 'CMV' named entity 'CMV infection' named entity 'serum' named entity 'tetramers' named entity 'cytomegalovirus' named entity 'cis' named entity 'inflammatory' named entity 'CMV' named entity 'BSA' named entity 'Basic Local Alignment Search Tool' named entity 'IL-4' named entity 'up-regulation' named entity 'avail' named entity 'MMP' named entity 'exosomes' named entity 'elution' named entity 'CD14' named entity 'CMV' named entity 'phenotype' named entity 'up-regulated' named entity 'bone marrow' named entity 'CD209' named entity 'Exosomes' named entity 'ligand' named entity 'elution' named entity 'France' named entity 'CMV' named entity 'homodimers' named entity 'supernatants' named entity 'Marimastat' named entity 'chemokine' named entity 'complement receptor 3' named entity 'IFN' named entity 'HIV' named entity 'transcription factor' named entity 'CXCL-8' named entity 'conjugated' named entity 'kDa' named entity 'alternative splicing' named entity 'virions' named entity 'blood-borne' named entity 'infection' named entity 'CD14' named entity 'Vancouver'

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