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Interferon-alpha promotes survival of human primary B-lymphocytes via phosphatidylinositol 3-kinase

K Ruuth1, L Carlsson, B Hallberg

  • 1Department of Cell and Molecular Biology, Umeå University, 901 87 Umeå, Sweden.

Biochemical and Biophysical Research Communications
|June 9, 2001
PubMed

Insights

Type I interferons (IFN) signal through novel pathways. IFN-alpha activates PI3-kinase-PKB/Akt, inhibiting B-lymphocyte apoptosis and downregulating p27/Kip1, suggesting a role in cell survival and proliferation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Type I interferons (IFN) are known for their antiviral and antiproliferative effects.
  • Established signaling pathways for these effects are well-documented.
  • The role of IFN-alpha in B-lymphocyte survival and cell cycle regulation requires further elucidation.

Purpose of the Study:

  • To investigate a novel signaling pathway for IFN-alpha.
  • To determine the role of PI3-kinase-PKB/Akt pathway in IFN-alpha-mediated effects.
  • To examine the impact of IFN-alpha on B-lymphocyte apoptosis and cell cycle inhibitors.

Main Methods:

  • Utilized phosphorylation assays to detect signaling events.
  • Employed PI3-kinase inhibitor LY294002 to block specific pathways.
  • Assessed spontaneous apoptosis in primary B-lymphocytes.
  • Analyzed the expression of p27/Kip1 in anti-IgM activated cells.

Main Results:

  • IFN-alpha induced rapid phosphorylation of PKB/Akt and its substrate forkhead.
  • PI3-kinase inhibitor LY294002 abolished these phosphorylations.
  • IFN-alpha inhibited spontaneous apoptosis of primary B-lymphocytes.
  • IFN-alpha stimulation downregulated p27/Kip1 expression in activated B-cells.

Conclusions:

  • IFN-alpha promotes survival of peripheral B-lymphocytes through the PI3-kinase-PKB/Akt pathway.
  • IFN-alpha signaling influences B-lymphocyte cell cycle regulation by downregulating p27/Kip1.
  • These findings reveal a novel mechanism for IFN-alpha in immune cell homeostasis.

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