New programming of IL-4 receptor signal transduction in activated T cells: Stat6 induction and Th2 differentiation mediated by IL-4Ralpha lacking cytoplasmic tyrosines

J Immunol. 2003 Aug 15;171(4):1891-900. doi: 10.4049/jimmunol.171.4.1891.

Abstract

Signaling by the IL-4 receptor alpha-chain (IL-4Ralpha) is a key determinant of the development of the Th2 lineage of effector T cells. Studies performed in tissue culture cell lines have indicated that tyrosines of the IL-4Ralpha cytoplasmic tail are necessary for the induction of Stat6, a transcription factor required for Th2 differentiation. Surprisingly, we have found that in activated T cells, IL-4Ralpha chains lacking all cytoplasmic tyrosines promote induction of this IL-4-specific transcription factor and efficient commitment to the Th2 lineage. Mutagenesis of a tyrosine-free cytoplasmic tail identifies a requirement for the serine-rich ID-1 region in this new program of IL-4R signal transduction observed in activated T cells. Additional findings suggest that an extracellular signal-regulated kinase pathway can be necessary and sufficient for the ability of such tyrosine-free IL-4Ralpha chains to mediate Stat6 induction. These results provide novel evidence that the molecular mechanisms by which a cytokine specifically induces a Stat transcription factor can depend on the activation state of T lymphoid cells. Furthermore, the data suggest that one pathway by which such new programming may be achieved is mediated by extracellular signal-regulated mitogen-activated protein kinases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Differentiation / genetics
  • Cell Differentiation / immunology
  • Cytoplasm / genetics
  • Cytoplasm / immunology
  • Cytoplasm / metabolism
  • Humans
  • Jurkat Cells
  • Lymphocyte Activation* / genetics
  • MAP Kinase Signaling System / genetics
  • MAP Kinase Signaling System / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Mutagenesis, Site-Directed
  • Peptide Fragments / deficiency
  • Peptide Fragments / genetics
  • Peptide Fragments / physiology
  • Protein Structure, Tertiary / genetics
  • Protein Structure, Tertiary / physiology
  • Protein Subunits / deficiency*
  • Protein Subunits / genetics
  • Protein Subunits / physiology
  • Receptors, Interleukin-4 / deficiency
  • Receptors, Interleukin-4 / genetics
  • Receptors, Interleukin-4 / physiology*
  • STAT6 Transcription Factor
  • Th2 Cells / cytology*
  • Th2 Cells / immunology
  • Th2 Cells / metabolism*
  • Trans-Activators / biosynthesis*
  • Tyrosine / deficiency*
  • Tyrosine / genetics

Substances

  • Peptide Fragments
  • Protein Subunits
  • Receptors, Interleukin-4
  • STAT6 Transcription Factor
  • STAT6 protein, human
  • Stat6 protein, mouse
  • Trans-Activators
  • Tyrosine