Source:http://linkedlifedata.com/resource/pubmed/id/17304625
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-3-5
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pubmed:abstractText |
In Th1 and Th2 memory lymphocytes, the genes for the cytokines interleukin (IL)-4 and interferon-gamma (IFN-gamma) are imprinted for expression upon restimulation. This cytokine memory is based on expression of the transcription factors T-bet for IFN-gamma, and GATA-3 for IL-4, and epigenetic modification of the cytokine genes. In Th2 cells, expression of the cytokine IL-10 is also induced by GATA-3. Here, we show that this induction is initially not accompanied by epigenetic modification of the IL-10 gene. Only after repeated restimulation of a memory Th2 cell in the presence of IL-4, extensive histone acetylation of the IL-10 gene is detectable. This epigenetic imprinting correlates with the development of a memory for IL-10 in repeatedly restimulated Th2 cells. In Th1 cells, IL-10 expression is induced by IL-12, but the IL-10 gene lacks detectable histone acetylation. Accordingly, IL-10 expression in restimulated memory Th1 cells remains conditional on the presence of IL-12. This finding defines a potential anti-inflammatory role for IL-12 in Th1 recall responses. While in primary Th1 responses IL-12 is required to induce expression of the pro-inflammatory cytokine IFN-gamma, in secondary Th1 responses IFN-gamma re-expression is independent of IL-12, which still is able to induce expression of the anti-inflammatory cytokine IL-10.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/GATA3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Gata3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
807-17
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17304625-Animals,
pubmed-meshheading:17304625-Cells, Cultured,
pubmed-meshheading:17304625-GATA3 Transcription Factor,
pubmed-meshheading:17304625-Genomic Imprinting,
pubmed-meshheading:17304625-Immunologic Memory,
pubmed-meshheading:17304625-Interleukin-10,
pubmed-meshheading:17304625-Interleukin-12,
pubmed-meshheading:17304625-Interleukin-4,
pubmed-meshheading:17304625-Lymphocyte Activation,
pubmed-meshheading:17304625-Mice,
pubmed-meshheading:17304625-Mice, Inbred BALB C,
pubmed-meshheading:17304625-Mice, Transgenic,
pubmed-meshheading:17304625-Promoter Regions, Genetic,
pubmed-meshheading:17304625-Protein Binding,
pubmed-meshheading:17304625-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:17304625-Th1 Cells
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pubmed:year |
2007
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pubmed:articleTitle |
Expression of IL-10 in Th memory lymphocytes is conditional on IL-12 or IL-4, unless the IL-10 gene is imprinted by GATA-3.
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pubmed:affiliation |
Deutsches Rheumaforschungszentrum Berlin, Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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