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

K Shimoda1, J van Deursen, M Y Sangster

  • 1Department of Biochemistry, St Jude Children's Research Hospital, Memphis, Tennessee 38105 USA.

Nature
|April 18, 1996
PubMed

Insights

Signal transducer and activator of transcription 6 (Stat6) mediates interleukin-4 (IL-4) functions. Stat6-null mice showed deficiencies in Th2 differentiation and IgE switching, confirming Stat6

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Signaling

Background:

  • Signal transducers and activators of transcription (Stats) mediate cytokine responses via tyrosine phosphorylation.
  • Signal transducer and activator of transcription 6 (Stat6) is activated by interleukin-4 (IL-4) and influences T-helper cell differentiation and immunoglobulin isotype switching.

Purpose of the Study:

  • To investigate the specific role of Stat6 in IL-4-mediated biological responses.
  • To generate and characterize Stat6-deficient mice (Stat6 -/-) to assess its non-redundant functions.

Main Methods:

  • Gene disruption in embryonic stem cells to create Stat6-null mice.
  • Analysis of lymphoid cell development and IL-4-dependent immune responses in Stat6 -/- mice.

Main Results:

  • Stat6-null mice were viable and exhibited normal naive lymphoid cell development.
  • Stat6 deficiency impaired IL-4-driven Th2 helper T-cell differentiation, cell surface marker expression, and immunoglobulin E (IgE) class switching.
  • IL-4-mediated proliferation was only partially affected in Stat6-null mice.

Conclusions:

  • Stat6 is essential for mediating key IL-4 functions, particularly Th2 differentiation and IgE class switching.
  • Stat6 does not appear to have a critical non-redundant role in normal mouse development or naive lymphocyte development.

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