Immunoglobulin-like transcripts ILT2, ILT3 and ILT7 are expressed by human dendritic cells and down-regulated following activation.
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 TNF alpha, 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.
Ju
Xin-Sheng
XS
Max-Delbrück-Center for Molecular Medicine, MDC, Robert-Rössle-Str. 10, 13092, Berlin, Germany.
Hacker
Christine
C
Scherer
Barbara
B
Redecke
Vanessa
V
Berger
Thomas
T
Schuler
Gerold
G
Wagner
Hermann
H
Lipford
Grayson B
GB
Zenke
Martin
M
D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism; D018952:Antigens, CD34 / Q000276:immunology; D023201:CD40 Ligand / Q000494:pharmacology; D002454:Cell Differentiation / Q000276:immunology; D018899:CpG Islands / Q000235:genetics; D004247:DNA / Q000235:genetics / Q000494:pharmacology; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D015232:Dinoprostone / Q000494:pharmacology; D015536:Down-Regulation / Q000187:drug effects; D005434:Flow Cytometry; D015870:Gene Expression / Q000187:drug effects; D020869:Gene Expression Profiling; D007375:Interleukin-1 / Q000494:pharmacology; D015850:Interleukin-6 / Q000494:pharmacology; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D008562:Membrane Glycoproteins; D009000:Monocytes / Q000166:cytology / Q000276:immunology; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods; D011070:Poly I-C / Q000494:pharmacology; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D011971:Receptors, Immunologic / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014158:Transcription, Genetic / Q000235:genetics*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D015703:Antigens, CD; D018952:Antigens, CD34; D007375:Interleukin-1; D015850:Interleukin-6; C488262:LILRA4 protein, human; C105299:LILRB1 protein, human; C107907:LILRB4 protein, human; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; D023201:CD40 Ligand; D004247:DNA; D015232:Dinoprostone; D011070:Poly I-C