Tumor-induced myeloid deviation: when myeloid-derived suppressor cells meet tumor-associated macrophages

J Clin Invest. 2015 Sep;125(9):3365-76. doi: 10.1172/JCI80006. Epub 2015 Sep 1.


The generation of an inflammatory environment is favorable and often decisive for the growth of both primary tumors and metastases. Tumor cells either express membrane molecules or release tumor-derived soluble factors able to alter myelopoiesis. Tumor-reprogrammed myeloid cells not only create a tolerogenic environment by blocking T cell functions and proliferation, but also directly drive tumor growth by promoting cancer stemness, angiogenesis, stroma deposition, epithelial-to-mesenchymal transition, and metastasis formation. In this Review, we discuss the interplay between immunosuppressive and protumoral myeloid cells and detail their immune-regulatory mechanisms, the molecular pathways involved in their differentiation, as well as their potential role as prognostic and diagnostic biomarkers and prospective targets for innovative approaches to treat tumor-bearing hosts.

Publication types

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

MeSH terms

  • Animals
  • Biomarkers, Tumor / immunology*
  • Cell Differentiation / immunology*
  • Epithelial-Mesenchymal Transition / immunology*
  • Humans
  • Immune Tolerance*
  • Macrophages / immunology*
  • Macrophages / pathology
  • Neoplasm Metastasis
  • Neoplasms / diagnosis
  • Neoplasms / immunology*
  • Neoplasms / pathology
  • Prognosis
  • T-Lymphocytes / immunology


  • Biomarkers, Tumor