Source:http://linkedlifedata.com/resource/pubmed/id/20739948
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
2011-1-13
|
pubmed:abstractText |
Molluscum contagiosum virus (MCV) infection induces self-limiting cutaneous lesions in an immunocompetent host that can undergo spontaneous regression preceded by local inflammation. On histology, a large majority of MCV-induced lesions are characterized by islands of hyperplastic epithelium containing infected keratinocytes and surrounded by scarce inflammatory infiltrate. However, spontaneous regression has been associated with the occurrence of a dense inflammatory reaction. By histology and immunohistochemistry, we identified MCV-induced lesions showing a dense inflammatory infiltrate associated with cell death in keratinocytes (inflammatory Molluscum contagiosum (I-MC)). In I-MC, hyperplastic keratinocytes were highly immunogenic as demonstrated by the expression of major histocompatibility complex class I and II molecules. Immune cell infiltration consisted of numerous cytotoxic T cells admixed with natural killer cells and plasmacytoid dendritic cells (PDCs). Accordingly, a type I IFN signature associated with PDC infiltration was demonstrated in both keratinocytes and inflammatory cells. Among the latter, a cell population resembling IFN-DC (CD123(+)CD11c(+)CD16(+)CD14(+)MxA(+)) was identified in proximity to islands of apoptotic keratinocytes. In vitro-generated IFN-DCs expressed a strong cytotoxic signature, as demonstrated by high levels of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FasL). This study establishes a previously unreported model to underpin the role of innate immune cells in viral immune surveillance.
|
pubmed:commentsCorrections | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11c,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-3 Receptor alpha Subunit,
http://linkedlifedata.com/resource/pubmed/chemical/TNF-Related Apoptosis-Inducing...,
http://linkedlifedata.com/resource/pubmed/chemical/TNFSF10 protein, human
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
1523-1747
|
pubmed:author |
pubmed-author:Calzavara-PintonPiergiacomoP,
pubmed-author:FacchettiFabioF,
pubmed-author:FisogniSimonaS,
pubmed-author:KutznerHeinzH,
pubmed-author:LeBoitPhilip EPE,
pubmed-author:LonardiSilviaS,
pubmed-author:RossiniCristinaC,
pubmed-author:SalogniLauraL,
pubmed-author:SchärerLeoL,
pubmed-author:SozzaniSilvanoS,
pubmed-author:VermiWilliamW
|
pubmed:issnType |
Electronic
|
pubmed:volume |
131
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
426-34
|
pubmed:meshHeading |
pubmed-meshheading:20739948-Animals,
pubmed-meshheading:20739948-Antigens, CD11c,
pubmed-meshheading:20739948-Apoptosis,
pubmed-meshheading:20739948-Biopsy,
pubmed-meshheading:20739948-Cell Communication,
pubmed-meshheading:20739948-Dendritic Cells,
pubmed-meshheading:20739948-Fas Ligand Protein,
pubmed-meshheading:20739948-Humans,
pubmed-meshheading:20739948-Immunity, Innate,
pubmed-meshheading:20739948-Inflammation,
pubmed-meshheading:20739948-Interferon Type I,
pubmed-meshheading:20739948-Interleukin-3 Receptor alpha Subunit,
pubmed-meshheading:20739948-Keratinocytes,
pubmed-meshheading:20739948-Molluscum Contagiosum,
pubmed-meshheading:20739948-Molluscum contagiosum virus,
pubmed-meshheading:20739948-Skin,
pubmed-meshheading:20739948-TNF-Related Apoptosis-Inducing Ligand
|
pubmed:year |
2011
|
pubmed:articleTitle |
Spontaneous regression of highly immunogenic Molluscum contagiosum virus (MCV)-induced skin lesions is associated with plasmacytoid dendritic cells and IFN-DC infiltration.
|
pubmed:affiliation |
Department of Pathology, University of Brescia, Brescia, Italy.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|