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A Novel Feeder-free System for Mass Production of Murine Natural Killer Cells In Vitro
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A Novel Feeder-free System for Mass Production of Murine Natural Killer Cells In Vitro

Published on: January 9, 2018

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Natural Killer Cells Control Tumor Growth by Sensing a Growth Factor

Alexander D Barrow1, Melissa A Edeling1, Vladimir Trifonov2

  • 1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Cell
|December 26, 2017
PubMed

Insights

Platelet-derived growth factor (PDGF)-DD promotes tumor growth, but its recognition by NKp44 on natural killer (NK) cells triggers anti-tumor immune responses. This interaction leads to cytokine release and tumor cell growth arrest, offering a potential therapeutic target.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Tumors often produce platelet-derived growth factor (PDGF)-DD, which drives cancer progression via PDGFRβ signaling.
  • This signaling pathway promotes cellular proliferation, epithelial-mesenchymal transition, stromal reaction, and angiogenesis.

Purpose of the Study:

  • To investigate the interaction between PDGF-DD and immune cells.
  • To determine the functional consequences of this interaction on anti-tumor immunity.

Main Methods:

  • Screening of a secretome library to identify PDGF-DD binding partners.
  • Analysis of NK cell activation and cytokine production upon PDGF-DD engagement.
  • Correlation of gene expression signatures with NKp44 (NCR2) expression and patient survival in glioblastoma.
  • In vivo studies using mouse models to assess tumor control.

Main Results:

  • The immunoreceptor NKp44, expressed on NK cells, was identified as a receptor for PDGF-DD.
  • Engagement of NKp44 by PDGF-DD stimulated NK cells to secrete interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α).
  • These secreted cytokines induced tumor cell growth arrest.
  • Higher NCR2 expression correlated with a specific transcriptional signature and improved survival in glioblastoma patients.
  • NKp44-expressing NK cells demonstrated enhanced control over PDGF-DD-expressing tumors in mice, further improved by CD96 blockade or CpG-oligonucleotide treatment.

Conclusions:

  • Tumor-derived PDGF-DD, while promoting tumor growth, also activates innate immune responses through NKp44.
  • NKp44-mediated signaling in NK cells triggers anti-tumor cytokine release and growth arrest.
  • This pathway represents a potential therapeutic strategy by harnessing innate immunity against PDGF-DD-expressing tumors.
Keywords:
NK cellNKp44PDGF-Dcancercell cyclecytokinesgrowth factorimmunosurveillanceinnate lymphoid cells

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