Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene

H. Shimoda, J. Van Deursen, M. Y. Sangster, S. R. Sarawar, R. T. Carson, R. A. Tripp, C. Chuo, F. W. Quelle, T. Nosaka, D. A.A. Vignali, P. C. Doherty, G. Grosveld, W. E. Paul, J. N. Ihle

Research output: Contribution to journalArticlepeer-review

1071 Scopus citations

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 responses. Stat6 is activated in response to interleukin (IL)-4 and may contribute to various functions including mitogenesis, T-helper cell differentiation and immunoglobulin isotype switching. To evaluate the role of Stat6, we generated Stat6-null mice (Stat6(-/-)) 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(-/-) 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.

Original languageEnglish (US)
Pages (from-to)630-633
Number of pages4
JournalNature
Volume380
Issue number6575
DOIs
StatePublished - May 1 1996

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene'. Together they form a unique fingerprint.

Cite this