Deconstructing innate immune signaling in myelodysplastic syndromes

Exp Hematol. 2015 Aug;43(8):587-598. doi: 10.1016/j.exphem.2015.05.016. Epub 2015 Jul 2.

Abstract

Overexpression of immune-related genes is widely reported in myelodysplastic syndromes (MDSs), and chronic immune stimulation increases the risk for developing MDS. Aberrant innate immune activation, such as that caused by increased toll-like receptor (TLR) signaling, in MDS can contribute to systemic effects on hematopoiesis, in addition to cell-intrinsic defects on hematopoietic stem/progenitor cell (HSPC) function. This review will deconstruct aberrant function of TLR signaling mediators within MDS HSPCs that may contribute to cell-intrinsic consequences on hematopoiesis and disease pathogenesis. We will discuss the contribution of chronic TLR signaling to the pathogenesis of MDS based on evidence from patients and mouse genetic models.

Publication types

  • Review

MeSH terms

  • Animals
  • Disease Models, Animal
  • Hematopoiesis / genetics
  • Hematopoiesis / immunology*
  • Hematopoietic Stem Cells / immunology*
  • Hematopoietic Stem Cells / pathology
  • Humans
  • Immunity, Innate*
  • Mice
  • Myelodysplastic Syndromes / genetics
  • Myelodysplastic Syndromes / immunology*
  • Myelodysplastic Syndromes / pathology
  • Signal Transduction / genetics
  • Signal Transduction / immunology*
  • Toll-Like Receptors / genetics
  • Toll-Like Receptors / immunology*

Substances

  • Toll-Like Receptors