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Interleukin-17D mediates tumor rejection through recruitment of natural killer cells

Timothy O'Sullivan1, Robert Saddawi-Konefka1, Emilie Gross1

  • 1Department of Pathology, University of California, San Diego, 9500 Gilman Drive MC 0612, La Jolla, CA 92093, USA.

Cell Reports
|May 6, 2014
PubMed

Insights

Interleukin 17D (IL-17D) is highly expressed in unedited tumors and enhances antitumor immunity by recruiting natural killer (NK) cells. Lower IL-17D levels in advanced human cancers suggest its therapeutic potential for cancer immune therapy.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Cancer immunoediting selects for tumor cells that evade immune responses.
  • While edited tumors can suppress immunity, the role of cytokines in unedited tumors is unclear.

Purpose of the Study:

  • To investigate whether unedited tumors produce cytokines that enhance antitumor immunity.
  • To explore the function of Interleukin 17D (IL-17D) in cancer immune responses.

Main Methods:

  • Gene microarray analysis to identify differentially expressed genes in unedited versus edited tumors.
  • Forced expression of IL-17D in edited tumor cells.
  • Assessment of immune cell recruitment (NK cells, macrophages) and activation.

Main Results:

  • IL-17D was highly expressed in unedited tumors but not in edited tumor cell lines.
  • Forced IL-17D expression in edited tumors led to tumor rejection.
  • IL-17D stimulated MCP-1 production, recruiting NK cells, which promoted M1 macrophage development and adaptive immunity.
  • Decreased IL-17D expression was observed in high-grade and metastatic human tumors.

Conclusions:

  • IL-17D plays a critical role in promoting antitumor immunity by orchestrating immune cell recruitment and activation.
  • IL-17D represents a potential therapeutic target for enhancing anti-cancer immune responses, particularly in tumors with low endogenous expression.

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