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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1997-11-7
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pubmed:abstractText |
CD4+ T cell differentiation into cells capable of producing IL-4 and IL-13 (Th2 cells) requires the presence of IL-4 and is STAT-6 dependent. Here we show that IL-4 is not required for IL-4 or IL-13 production by Th2 cells. Anti-IL-4 or anti-IL-4R Ab did not diminish IL-4 production by Th2 cells in response to TCR-mediated stimulation, nor did IL-4 enhance IL-4 production in response to stimulation of Th2 cells with limiting amounts of Ag. Th2 cells prepared from IL-4 knockout mice were capable of producing IL-13 mRNA in response to stimulation with immobilized anti-CD3. IL-4 did not increase IL-13 mRNA expression. Despite the failure of IL-4 to effect IL-4 production by primed Th2 cells, a STAT-6 binding element was demonstrated in the IL-4 promoter. The authenticity of this element was demonstrated by oligonucleotide competition, by supershifting with anti-STAT-6 Ab, and by IL-4-inducible effects on transcription of a reporter gene under the control of a multimerized element fused to an IL-4 minimal promoter. Nonetheless, an IL-4 promoter construct lacking the STAT-6 binding element was as effective as a construct containing this element in anti-CD3-induced reporter transcription. Thus, this element, if biologically active, must function at a step in T cell responsiveness distinct from the acute production of IL-4 by Th2 cells in response to Ag or anti-CD3.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/STAT6 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat6 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
159
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3731-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:9378959-Animals,
pubmed-meshheading:9378959-Autocrine Communication,
pubmed-meshheading:9378959-Cell Differentiation,
pubmed-meshheading:9378959-Cells, Cultured,
pubmed-meshheading:9378959-Feedback,
pubmed-meshheading:9378959-Interleukin-13,
pubmed-meshheading:9378959-Interleukin-4,
pubmed-meshheading:9378959-Mice,
pubmed-meshheading:9378959-Mice, Inbred A,
pubmed-meshheading:9378959-Mice, Inbred C57BL,
pubmed-meshheading:9378959-Mice, Knockout,
pubmed-meshheading:9378959-Mice, Transgenic,
pubmed-meshheading:9378959-Promoter Regions, Genetic,
pubmed-meshheading:9378959-RNA, Messenger,
pubmed-meshheading:9378959-Receptors, Antigen, T-Cell,
pubmed-meshheading:9378959-STAT6 Transcription Factor,
pubmed-meshheading:9378959-Signal Transduction,
pubmed-meshheading:9378959-Th2 Cells,
pubmed-meshheading:9378959-Trans-Activators,
pubmed-meshheading:9378959-Transcription, Genetic
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pubmed:year |
1997
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pubmed:articleTitle |
IL-4 and IL-13 production in differentiated T helper type 2 cells is not IL-4 dependent.
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pubmed:affiliation |
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-1892, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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