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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2011-2-18
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pubmed:abstractText |
In this study, we investigated the role of a transcription factor, PU.1, in the regulation of CD80 and CD86 expression in dendritic cells (DCs). A chromatin immunoprecipitation assay revealed that PU.1 is constitutively bound to the CD80 and CD86 promoters in bone marrow-derived DCs. In addition, co-expression of PU.1 resulted in the transactivation of the CD80 and CD86 promoters in a reporter assay. The binding of PU.1 to cis-enhancing regions was confirmed by electromobility gel-shift assay. As expected, inhibition of PU.1 expression by short interfering RNA (siRNA) in bone marrow-derived DCs resulted in marked down-regulation of CD80 and CD86 expression. Moreover, overexpression of PU.1 in murine bone marrow-derived lineage-negative cells induced the expression of CD80 and CD86 in the absence of monocyte/DC-related growth factors and/or cytokines. Based on these results, we conclude that PU.1 is a critical factor for the expression of CD80 and CD86. We also found that subcutaneous injection of PU.1 siRNA or topical application of a cream-emulsified PU.1 siRNA efficiently inhibited murine contact hypersensitivity. Our results suggest that PU.1 is a potential target for the treatment of immune-related diseases.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Cd86 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/proto-oncogene protein Spi-1
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1528-0020
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
17
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pubmed:volume |
117
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2211-22
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pubmed:meshHeading |
pubmed-meshheading:21119111-Administration, Topical,
pubmed-meshheading:21119111-Animals,
pubmed-meshheading:21119111-Antigens, CD80,
pubmed-meshheading:21119111-Antigens, CD86,
pubmed-meshheading:21119111-Base Sequence,
pubmed-meshheading:21119111-Binding Sites,
pubmed-meshheading:21119111-DNA, Complementary,
pubmed-meshheading:21119111-Dendritic Cells,
pubmed-meshheading:21119111-Dermatitis, Contact,
pubmed-meshheading:21119111-Down-Regulation,
pubmed-meshheading:21119111-Female,
pubmed-meshheading:21119111-Mice,
pubmed-meshheading:21119111-Mice, Inbred BALB C,
pubmed-meshheading:21119111-Molecular Sequence Data,
pubmed-meshheading:21119111-Promoter Regions, Genetic,
pubmed-meshheading:21119111-Proto-Oncogene Proteins,
pubmed-meshheading:21119111-RNA, Small Interfering,
pubmed-meshheading:21119111-Trans-Activators,
pubmed-meshheading:21119111-Transcription Initiation Site,
pubmed-meshheading:21119111-Transcriptional Activation
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pubmed:year |
2011
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pubmed:articleTitle |
Critical role of transcription factor PU.1 in the expression of CD80 and CD86 on dendritic cells.
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pubmed:affiliation |
Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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