Abstract
In this study, we report that an acute phase reactant, serum amyloid A (SAA), strongly inhibits dendritic cell differentiation induced by GM-CSF plus IL-4. SAA markedly decreased the expression of MHCII and CD11c. Moreover, SAA decreased cell surface GM-CSF receptor expression. SAA also decreased the expression of PU.1 and C/EBPα, which play roles in the expression of GM-CSF receptor. This inhibitory response by SAA is partly mediated by the well-known SAA receptors, Toll-like receptor 2 and formyl peptide receptor 2. Taken together, we suggest a novel insight into the inhibitory role of SAA in dendritic cell differentiation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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CCAAT-Enhancer-Binding Proteins / genetics
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CCAAT-Enhancer-Binding Proteins / metabolism
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CD11c Antigen / genetics
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CD11c Antigen / metabolism
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Cell Differentiation*
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Dendritic Cells / cytology*
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Dendritic Cells / metabolism*
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Humans
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Macrophages / metabolism*
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Male
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Mice
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Mice, Inbred C57BL
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Primary Cell Culture
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism
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Receptors, Formyl Peptide / genetics
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Receptors, Formyl Peptide / metabolism*
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Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / genetics
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Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / metabolism*
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Serum Amyloid A Protein / genetics
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Serum Amyloid A Protein / metabolism*
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Toll-Like Receptor 2 / genetics
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Toll-Like Receptor 2 / metabolism*
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Trans-Activators / genetics
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Trans-Activators / metabolism
Substances
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CCAAT-Enhancer-Binding Proteins
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CD11c Antigen
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MHC class II transactivator protein
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Nuclear Proteins
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Proto-Oncogene Proteins
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Receptors, Formyl Peptide
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Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
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Serum Amyloid A Protein
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Tlr2 protein, mouse
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Toll-Like Receptor 2
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Trans-Activators
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formyl peptide receptor 2, mouse
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proto-oncogene protein Spi-1