The Yin-Yang of tumor-associated macrophages in neoplastic progression and immune surveillance

Immunol Rev. 2008 Apr;222:155-61. doi: 10.1111/j.1600-065X.2008.00607.x.

Abstract

An intrinsic (oncogene-driven) pathway and an extrinsic (microenvironment-driven) pathway connect inflammatory reactions and cancer. M2-polarized tumor-associated macrophages and the related myeloid-derived suppressor cells are key prototypic components of smoldering inflammation driving neoplastic progression. However, mononuclear phagocytes can exert anti-tumor activity by killing tumor cells and eliciting tissue disruptive reactions (M1), a likely scenario in the early phases of carcinogenesis of immunogenic tumors and following therapeutic intervention. Shifting the macrophage balance represents a viable therapeutic target. Herein, the 'macrophage balance' is discussed in the context of the apparent paradox of tumor promotion by innate immunity-driven inflammation and the seemingly opposed tumor surveillance by adaptive immune responses.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic / immunology
  • Cytokines / immunology
  • Disease Progression
  • Female
  • Gonadal Steroid Hormones / immunology
  • Humans
  • Immunity, Innate
  • Immunologic Surveillance*
  • Inflammation*
  • Macrophage Activation / immunology*
  • Macrophages / immunology*
  • Macrophages / pathology*
  • Male
  • Matrix Metalloproteinases / immunology
  • Mice
  • Myeloid Cells / immunology
  • Myeloid Cells / pathology
  • Neoplasms / blood supply
  • Neoplasms / immunology*
  • Neoplasms / pathology*
  • Neovascularization, Pathologic / immunology
  • Phagocytosis / immunology
  • Rats
  • Signal Transduction / immunology
  • Tumor Escape
  • Vascular Endothelial Growth Factor A / immunology

Substances

  • Cytokines
  • Gonadal Steroid Hormones
  • Vascular Endothelial Growth Factor A
  • Matrix Metalloproteinases