Myeloid-derived suppressor cells and tumor: Current knowledge and future perspectives

J Cell Physiol. 2019 Jul;234(7):9966-9981. doi: 10.1002/jcp.27923. Epub 2018 Dec 7.

Abstract

The immunosuppressive features of tumor lesions participate not only as one of the major players inducing cancer progression but also a big challenge for effective immunotherapy. It has been found that immunosuppression associated with chronic inflammatory factors, such as growth factors, cytokines, and chemokines is generated by stroma and tumor cells. Chronic and exhaustive secretion of these mediators triggers the generation of myeloid-derived suppressor cells (MDSCs) demonstrating one of the key players engaged in tumor immunosuppression. In point of fact, direct cell-to-cell contact is a prerequisite for immunosuppressive functions of MDSCs. From the clinical perspective, the frequency of peripheral blood MDSCs is correlated with clinical stage and therapeutic response in various cancers. Furthermore, MDSCs are involved in chemoresistant settings. Altogether, it is a rational therapeutic approach to block the fierce cycle in which MDSCs are developed and infiltrated to favor cancer progression. In this review, we will summarize recent findings of MDSCs in tumor progression and discuss potential therapeutic strategies that could be evaluated in future clinical trials.

Keywords: immunosuppression; inflammation; myeloid-derived suppressor cells; tumor.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / therapeutic use
  • Cell Communication
  • Disease Progression
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Inflammation Mediators / metabolism
  • Myeloid-Derived Suppressor Cells / drug effects
  • Myeloid-Derived Suppressor Cells / immunology
  • Myeloid-Derived Suppressor Cells / metabolism*
  • Myeloid-Derived Suppressor Cells / pathology
  • Neoplasms / drug therapy
  • Neoplasms / immunology
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Signal Transduction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Tumor Escape* / drug effects
  • Tumor Microenvironment*

Substances

  • Antineoplastic Agents
  • Inflammation Mediators
  • Transcription Factors