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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1996-6-27
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pubmed:abstractText |
Interleukin-4 (IL-4) stimulation of cells leads to the activation of multiple signaling pathways, one of which involves Stat6. We have generated Stat6-deficient mice by gene targeting in embryonic stem cells to determine the role of this transcription factor in mediating the biologic functions of IL-4. IL-4-induced increases in the cell surface expression of both MHC class II antigens and IL-4 receptor are completely abrogated, and lymphocytes from Stat6-deficient animals fail to proliferate in response to IL-4. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. In addition, Stat6-deficient T lymphocytes fail to differentiate into Th2 cells in response to either IL-4 or Il-13. These results demonstrate that, despite the existence of multiple signaling pathways activated by IL-4, Stat6 is essential for mediating responses to IL-4 lymphocytes.
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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 |
Mar
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pubmed:issn |
1074-7613
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
313-9
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:8624821-Animals,
pubmed-meshheading:8624821-Cell Differentiation,
pubmed-meshheading:8624821-Immunoglobulin E,
pubmed-meshheading:8624821-Interleukin-4,
pubmed-meshheading:8624821-Lymphocyte Activation,
pubmed-meshheading:8624821-Membrane Proteins,
pubmed-meshheading:8624821-Mice,
pubmed-meshheading:8624821-Mice, Mutant Strains,
pubmed-meshheading:8624821-STAT6 Transcription Factor,
pubmed-meshheading:8624821-Signal Transduction,
pubmed-meshheading:8624821-T-Lymphocyte Subsets,
pubmed-meshheading:8624821-Th2 Cells,
pubmed-meshheading:8624821-Trans-Activators,
pubmed-meshheading:8624821-Up-Regulation
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pubmed:year |
1996
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pubmed:articleTitle |
Stat6 is required for mediating responses to IL-4 and for development of Th2 cells.
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pubmed:affiliation |
Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
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pubmed:publicationType |
Journal Article
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