History of myeloid-derived suppressor cells

Nat Rev Cancer. 2013 Oct;13(10):739-52. doi: 10.1038/nrc3581.

Abstract

Tumour-induced granulocytic hyperplasia is associated with tumour vasculogenesis and escape from immunity via T cell suppression. Initially, these myeloid cells were identified as granulocytes or monocytes; however, recent studies have revealed that this hyperplasia is associated with populations of multipotent progenitor cells that have been identified as myeloid-derived suppressor cells (MDSCs). The study of MDSCs has provided a wealth of information regarding tumour pathobiology, has extended our understanding of neoplastic progression and has modified our approaches to immune adjuvant therapy. In this Timeline article, we discuss the history of MDSCs, their influence on tumour progression and metastasis, and the crosstalk between tumour cells, MDSCs and the host macroenvironment.

Publication types

  • Historical Article
  • Review

MeSH terms

  • Animals
  • Antigens, Differentiation / analysis
  • Antigens, Neoplasm / analysis
  • Cell Biology / history*
  • Cell Differentiation
  • Cell Lineage
  • Chemokines / physiology
  • Hematopoiesis, Extramedullary
  • Hematopoietic Stem Cell Mobilization / adverse effects
  • History, 20th Century
  • History, 21st Century
  • Humans
  • Leukemoid Reaction / pathology
  • Medical Oncology / history*
  • Mice
  • Molecular Targeted Therapy
  • Multipotent Stem Cells / cytology*
  • Multipotent Stem Cells / drug effects
  • Multipotent Stem Cells / physiology
  • Myeloid Cells / cytology
  • Myeloid Cells / drug effects
  • Myeloid Cells / physiology
  • Myeloid Progenitor Cells / cytology*
  • Myeloid Progenitor Cells / drug effects
  • Myeloid Progenitor Cells / physiology
  • Neoplasm Invasiveness / physiopathology
  • Neoplasm Metastasis
  • Neoplasms / immunology
  • Neoplasms / pathology*
  • Neovascularization, Pathologic / physiopathology
  • Tumor Burden
  • Tumor Escape
  • Tumor Microenvironment

Substances

  • Antigens, Differentiation
  • Antigens, Neoplasm
  • Chemokines