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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2007-4-9
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pubmed:abstractText |
T cell sensitivity to antigen is intrinsically regulated during maturation to ensure proper development of immunity and tolerance, but how this is accomplished remains elusive. Here we show that increasing miR-181a expression in mature T cells augments the sensitivity to peptide antigens, while inhibiting miR-181a expression in the immature T cells reduces sensitivity and impairs both positive and negative selection. Moreover, quantitative regulation of T cell sensitivity by miR-181a enables mature T cells to recognize antagonists-the inhibitory peptide antigens-as agonists. These effects are in part achieved by the downregulation of multiple phosphatases, which leads to elevated steady-state levels of phosphorylated intermediates and a reduction of the T cell receptor signaling threshold. Importantly, higher miR-181a expression correlates with greater T cell sensitivity in immature T cells, suggesting that miR-181a acts as an intrinsic antigen sensitivity "rheostat" during T cell development.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0092-8674
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pubmed:author |
pubmed-author:BraichRaviR,
pubmed-author:ChauJacquelineJ,
pubmed-author:ChenChang-ZhengCZ,
pubmed-author:DavisMark MMM,
pubmed-author:EbertPeter J RPJ,
pubmed-author:KleinLawrence OLO,
pubmed-author:LiQi-JingQJ,
pubmed-author:LiuGwenG,
pubmed-author:ManoharanMuthiahM,
pubmed-author:MinHyeyoungH,
pubmed-author:SkarePetraP,
pubmed-author:SoutschekJuergenJ,
pubmed-author:SylvesterGiselleG
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pubmed:issnType |
Print
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pubmed:day |
6
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pubmed:volume |
129
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
147-61
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pubmed:dateRevised |
2011-3-2
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pubmed:meshHeading |
pubmed-meshheading:17382377-Animals,
pubmed-meshheading:17382377-Antigen-Presenting Cells,
pubmed-meshheading:17382377-Cell Differentiation,
pubmed-meshheading:17382377-Cell Line, Tumor,
pubmed-meshheading:17382377-Cytochromes c,
pubmed-meshheading:17382377-Down-Regulation,
pubmed-meshheading:17382377-Gene Expression Regulation,
pubmed-meshheading:17382377-Mice,
pubmed-meshheading:17382377-Mice, Transgenic,
pubmed-meshheading:17382377-MicroRNAs,
pubmed-meshheading:17382377-Moths,
pubmed-meshheading:17382377-NIH 3T3 Cells,
pubmed-meshheading:17382377-Oligonucleotides, Antisense,
pubmed-meshheading:17382377-Organ Culture Techniques,
pubmed-meshheading:17382377-Peptides,
pubmed-meshheading:17382377-Phosphoric Monoester Hydrolases,
pubmed-meshheading:17382377-Receptors, Antigen, T-Cell,
pubmed-meshheading:17382377-Signal Transduction,
pubmed-meshheading:17382377-T-Lymphocytes,
pubmed-meshheading:17382377-Thymus Gland
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pubmed:year |
2007
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pubmed:articleTitle |
miR-181a is an intrinsic modulator of T cell sensitivity and selection.
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pubmed:affiliation |
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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