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Stat6 is required for mediating responses to IL-4 and for development of Th2 cells.

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.

Pubmed ID: 8624821

Authors

  • Kaplan MH
  • Schindler U
  • Smiley ST
  • Grusby MJ

Journal

Immunity

Publication Data

March 27, 1996

Associated Grants

None

Mesh Terms

  • Animals
  • Cell Differentiation
  • Immunoglobulin E
  • Interleukin-4
  • Lymphocyte Activation
  • Membrane Proteins
  • Mice
  • Mice, Mutant Strains
  • STAT6 Transcription Factor
  • Signal Transduction
  • T-Lymphocyte Subsets
  • Th2 Cells
  • Trans-Activators
  • Up-Regulation