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Myeloid cells migrate in response to IL-24

Krisztina Buzas1, Joost J Oppenheim, O M Zack Howard

  • 1Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, National Cancer Institute-Frederick, Center for Cancer Research, Frederick, MD 21702, USA.

Cytokine
|June 28, 2011
PubMed

Insights

Interleukin-24 (IL-24) promotes the migration of human immune cells, including monocytes and neutrophils. This cytokine activates signaling pathways, potentially contributing to its anti-cancer effects by attracting myeloid cells.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cancer Research

Background:

  • Interleukin-24 (IL-24), a member of the IL-10 cytokine family, exhibits anti-tumor activity.
  • IL-24 is produced by immune tissues and its expression is inducible in human peripheral blood mononuclear cells.
  • The specific response of immune cells to IL-24 remains largely uncharacterized.

Purpose of the Study:

  • To investigate the chemotactic effects of IL-24 on human immune cells.
  • To identify the signaling pathways and receptors involved in IL-24-induced immune cell migration.

Main Methods:

  • Recombinant human IL-24 was used to stimulate human monocytes and neutrophils in vitro.
  • An in vivo chemotaxis model was employed to assess IL-24's effect on myeloid cell attraction.
  • Signaling pathway inhibitors (pertussis toxin, MEK, JAK inhibitors) were used to probe IL-24's mechanism of action.

Main Results:

  • IL-24 demonstrated in vitro chemotactic activity, inducing migration of human monocytes and neutrophils.
  • In vivo models confirmed that IL-24 attracts CD11b positive myeloid cells.
  • IL-24-induced monocyte migration was significantly reduced by pertussis toxin, MEK, and JAK inhibitors, implicating G-protein coupled receptors and associated signaling cascades.

Conclusions:

  • IL-24 elicits migration of myeloid cells through activation of multiple signaling cascades.
  • These findings suggest a mechanism by which IL-24's anti-cancer properties may be mediated via immune cell recruitment.

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