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Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia
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Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia

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Mechanism regulating reactive oxygen species in tumor-induced myeloid-derived suppressor cells

Cesar A Corzo1, Matthew J Cotter, Pingyan Cheng

  • 1H. Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, FL, 33612, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|April 22, 2009
PubMed

Insights

Myeloid-derived suppressor cells (MDSC) use reactive oxygen species (ROS) to suppress immune responses in cancer. Blocking NADPH oxidase (NOX2) in MDSC halts this suppression and promotes cell differentiation.

Area of Science:

  • Immunology
  • Cancer Biology
  • Cellular Biology

Background:

  • Myeloid-derived suppressor cells (MDSC) are key players in immune suppression within the tumor microenvironment.
  • Reactive oxygen species (ROS) are implicated as a major mechanism for MDSC-mediated immune suppression.
  • The precise molecular mechanisms underlying ROS production by MDSC were previously unclear.

Purpose of the Study:

  • To elucidate the mechanism by which MDSC produce ROS.
  • To investigate the role of NADPH oxidase (NOX2) in MDSC function.
  • To explore the therapeutic potential of targeting NOX2 in cancer.

Main Methods:

  • Quantification of ROS production in MDSC from various tumor models and head and neck cancer patients.
  • Analysis of NOX2 subunit expression (p47(phox), gp91(phox)) in MDSC.
  • Investigation of STAT3's role in regulating NOX2 expression.
  • Assessment of T cell suppression and MDSC differentiation in the absence of NOX2 activity.

Main Results:

  • MDSC exhibited significantly increased ROS production across seven tumor models and in head and neck cancer patients.
  • Upregulated activity and expression of NOX2 subunits in MDSC were identified as the source of increased ROS.
  • STAT3 was found to control the expression of NOX2 subunits in MDSC.
  • Inhibition of NOX2 activity resulted in loss of T cell suppressive function and promoted MDSC differentiation into mature myeloid cells.

Conclusions:

  • MDSC-induced immune suppression is critically dependent on ROS production mediated by NOX2.
  • STAT3 is a key regulator of NOX2 expression in MDSC.
  • Targeting NOX2 in MDSC represents a potential therapeutic strategy to restore anti-tumor immunity.

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