Journal article
Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted stat6 gene
Nature (London), Vol.380(6575), pp.630-633
1996
DOI: 10.1038/380630a0
PMID: 8602264
Abstract
SIGNAL transducers and activators of transcription (Stats) are activated by tyrosine phosphorylation in response to cytokines, and are thought to mediate many of their functional responses1–4. Stat6 is activated in response to interleukin (IL)-4 (refs 5,6) and may contribute to various functions including mitogenesis, T-helper cell differentiation and immunoglobulin i so type switching7. To evaluate the role of Stat6, we generated Stat6-null mice (Stat6-l-) by gene disruption in embryonic stem cells. The mice were viable, indicating the lack of a non-redundant function in normal development. Although naive lymphoid cell development was normal, Stat6-l- mice were deficient in IL-4-mediated functions including Th2 helper T-cell differentiation, expression of cell surface markers, and immunoglobulin class switching to IgE. In contrast, IL-4-mediated proliferation was only partly affected.
Details
- Title: Subtitle
- Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted stat6 gene
- Creators
- Kazuya Shimoda - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesFrederick W Quelle - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesJ VAN DEURSEN - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesP. C DOHERTY - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesG GROSVELD - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesW. E PAUL - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesJ. N IHLE - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesMark Y Sangster - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesSally R Sarawar - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesRichard T Carson - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesRalph A Tripp - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesCharles Chu - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesTetsuya Nosaka - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United StatesDario A A Vignali - Department of Biochemistry, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, Tennessee 38105, United States
- Resource Type
- Journal article
- Publication Details
- Nature (London), Vol.380(6575), pp.630-633
- Publisher
- Nature Publishing; London
- DOI
- 10.1038/380630a0
- PMID
- 8602264
- ISSN
- 0028-0836
- eISSN
- 1476-4687
- Language
- English
- Date published
- 1996
- Academic Unit
- Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040536502771
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