A promiscuous liaison between IL-15 receptor and Axl receptor tyrosine kinase in cell death control

EMBO J. 2005 Dec 21;24(24):4260-70. doi: 10.1038/sj.emboj.7600874. Epub 2005 Nov 24.

Abstract

Discrimination between cytokine receptor and receptor tyrosine kinase (RTK) signaling pathways is a central paradigm in signal transduction research. Here, we report a 'promiscuous liaison' between both receptors that enables interleukin (IL)-15 to transactivate the signaling pathway of a tyrosine kinase. IL-15 protects murine L929 fibroblasts from tumor necrosis factor alpha (TNFalpha)-induced cell death, but fails to rescue them upon targeted depletion of the RTK, Axl; however, Axl-overexpressing fibroblasts are TNFalpha-resistant. IL-15Ralpha and Axl colocalize on the cell membrane and co-immunoprecipitate even in the absence of IL-15, whereby the extracellular part of Axl proved to be essential for Axl/IL-15Ralpha interaction. Most strikingly, IL-15 treatment mimics stimulation by the Axl ligand, Gas6, resulting in a rapid tyrosine phosphorylation of both Axl and IL-15Ralpha, and activation of the phosphatidylinositol 3-kinase/Akt pathway. This is also seen in mouse embryonic fibroblasts from wild-type but not Axl-/- or IL-15Ralpha-/- mice. Thus, IL-15-induced protection from TNFalpha-mediated cell death involves a hitherto unknown IL-15 receptor complex, consisting of IL-15Ralpha and Axl RTK, and requires their reciprocal activation initiated by ligand-induced IL-15Ralpha.

Publication types

  • Research Support, Non-U.S. Gov't
  • Retracted Publication

MeSH terms

  • Animals
  • Axl Receptor Tyrosine Kinase
  • Cell Death
  • Cell Differentiation
  • Cell Line
  • Cell Separation
  • Ceramides / metabolism
  • Cytokines / metabolism
  • Dendritic Cells / cytology
  • Enzyme Activation
  • Enzyme-Linked Immunosorbent Assay
  • Fibroblasts / metabolism
  • Flow Cytometry
  • Humans
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Interleukin-15 / metabolism
  • Interleukin-15 / physiology*
  • Ligands
  • Mice
  • Mice, Transgenic
  • Microscopy, Confocal
  • Models, Biological
  • Oncogene Proteins / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Binding
  • Proto-Oncogene Proteins
  • RNA, Small Interfering / metabolism
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Receptors, Interleukin-15
  • Receptors, Interleukin-2 / chemistry
  • Receptors, Interleukin-2 / metabolism*
  • Recombinant Fusion Proteins / chemistry
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Transcriptional Activation
  • Transfection
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Ceramides
  • Cytokines
  • IL15RA protein, human
  • Il15ra protein, mouse
  • Intercellular Signaling Peptides and Proteins
  • Interleukin-15
  • Ligands
  • Oncogene Proteins
  • Proto-Oncogene Proteins
  • RNA, Small Interfering
  • Receptors, Interleukin-15
  • Receptors, Interleukin-2
  • Recombinant Fusion Proteins
  • Tumor Necrosis Factor-alpha
  • growth arrest-specific protein 6
  • Phosphatidylinositol 3-Kinases
  • Receptor Protein-Tyrosine Kinases
  • Axl Receptor Tyrosine Kinase