English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/162902
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

Title

Regulated expression of the pathogen receptor dendritic cell-specific intercellular adhesion molecule 3 (ICAM-3)-grabbing nonintegrin in THP-1 human leukemic cells, monocytes, and macrophages

AuthorsPuig-Kröger, Amaya ; Serrano-Gómez, Diego; Caparrós, Esther; Domínguez-Soto, Ángeles ; Relloso, Miguel; Colmenares, María ; Sánchez-Sánchez, Noelia; Rivas, Luis ; Corbí, Angel L.
Issue Date11-Jun-2004
PublisherAmerican Society for Biochemistry and Molecular Biology
CitationJ Biol Chem 279(24):25680-8 (2004)
AbstractDendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) is a type II C-type lectin that functions as an adhesion receptor and mediates binding and internalization of pathogens such as virus (human immunodeficiency virus, hepatitis C), bacteria (Mycobacterium), fungi, and parasites. DC-SIGN expression in vivo is primarily restricted to interstitial dendritic cells (DC) and certain tissue macrophages. We now report that leukemic THP-1 cells, widely used as a model for monocyte-macrophage differentiation, express very low basal levels of DC-SIGN and that DC-SIGN expression in THP-1 cells is regulated during differentiation. Differentiation-inducing agents (phorbol ester, bryostatin) conveyed THP-1 cells with the ability to up-regulate DC-SIGN mRNA levels and cell surface expression in response to interleukin-4 (IL-4) or IL-13. DC-SIGN up-regulation required a functional JAK-STAT signaling pathway, was inhibited in the presence of lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNF-alpha), and conferred THP-1 cells with increased pathogen recognition and T cell stimulatory capabilities. The up-regulation of DC-SIGN on THP-1 cells resembles its inducible expression on monocytes and macrophages, where DC-SIGN expression is also induced by IL-4/IL-13 and negatively regulated by TNF-alpha, LPS, and vitamin D(3). These results point to THP-1 cells as a useful cellular system to characterize the pathogen-binding capabilities of DC-SIGN and to dissect the molecular mechanisms that control its regulated and tissue-specific expression in myeloid dendritic cells, and the results suggest that DC-SIGN constitutes a marker for both DC and alternatively activated macrophages.
Description9 p.-9 fig. Puig-Kröger, Amaya et al.
Publisher version (URL)http://dx.doi.org/10.1074/jbc.M311516200
URIhttp://hdl.handle.net/10261/162902
DOI10.1074/jbc.M311516200
ISSN0021-9258
E-ISSN1083-351X
Appears in Collections:(CIB) Artículos
Files in This Item:
File Description SizeFormat 
J. Biol. Chem.-2004-Puig-Kröger-25680-8.pdfArtículo principal557,34 kBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.