1. Deconstructing innate immune signaling in myelodysplastic syndromes.
- Author
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Varney ME, Melgar K, Niederkorn M, Smith M, Barreyro L, and Starczynowski DT
- Subjects
- Animals, Disease Models, Animal, Hematopoiesis genetics, Hematopoietic Stem Cells pathology, Humans, Mice, Myelodysplastic Syndromes genetics, Myelodysplastic Syndromes pathology, Signal Transduction genetics, Toll-Like Receptors genetics, Hematopoiesis immunology, Hematopoietic Stem Cells immunology, Immunity, Innate, Myelodysplastic Syndromes immunology, Signal Transduction immunology, Toll-Like Receptors immunology
- 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., (Copyright © 2015 ISEH - International Society for Experimental Hematology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2015
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