| Literature DB >> 26143580 |
Madeline Niederkorn1,2, Molly Smith1,2, Laura Barreyro1, Melinda E Varney1, Katelyn Melgar1,3, Daniel T Starczynowski1,2.
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.Entities:
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Year: 2015 PMID: 26143580 PMCID: PMC4635673 DOI: 10.1016/j.exphem.2015.05.016
Source DB: PubMed Journal: Exp Hematol ISSN: 0301-472X Impact factor: 3.084