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Immunoglobulin-like transcripts ILT2, ILT3 and ILT7 are expressed by human dendritic cells and down-regulated following activation

Item Type:Article
Title:Immunoglobulin-like transcripts ILT2, ILT3 and ILT7 are expressed by human dendritic cells and down-regulated following activation
Creators Name:Ju, X.S. and Hacker, C. and Scherer, B. and Redecke, V. and Berger, T. and Schuler, G. and Wagner, H. and Lipford, G.B. and Zenke, M.
Abstract:Immunoglobulin-like transcripts (ILT) represent novel immunoglobulin superfamily receptors that are expressed in myeloid, lymphoid and dendritic cells (DC). Here, we studied by gene expression profiling with DNA microarrays ILT expression in different DC subsets, including plasmacytoid DC (PDC), monocyte-derived DC (Mo-DC) and DC obtained by in vitro differentiation from CD34 + progenitor cells, and DC activated in the presence of different activating agents. ILT2 and ILT3 were expressed in PDC, Mo-DC and DC obtained from CD34 + cells. ILT7 mRNA was present in PDC, but absent in Mo-DC and DC obtained from CD34 + cells, indicating that ILT7 mRNA expression seems to be a marker for PDC. CpG-DNA and inflammatory stimuli, such as TNFα, prostaglandin E2 (PGE2) and soluble CD40 ligand (sCD40L), and different combinations thereof are frequently employed for DC activation. Here, we demonstrate that ILT2 and ILT3 expression is down-regulated following DC activation by CpG-DNA and inflammatory stimuli at both mRNA and protein levels. Thus, activation of human DC with such stimuli involves down-regulation of inhibitory ILT2 and ILT3 receptors, and this could represent a novel mechanism contributing to DC activation.
Keywords:CpG-DNA, DC, Dendritic Cells, ILT, Immunoglobulin-Like Transcripts, Inflammatory Stimuli, Leukocyte Immunoglobulin-Like Receptors, LIR, Mo-DC, Monocyte-Derived Dendritic Cells, PDC, Plasmacytoid Dendritic Cells
Source:Gene
ISSN:0378-1119
Publisher:Elsevier
Volume:331
Number:1-2
Page Range:159-164
Date:28 April 2004
Official Publication:https://doi.org/10.1016/j.gene.2004.02.018
PubMed:View item in PubMed

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