期刊
EXPERIMENTAL HEMATOLOGY
卷 43, 期 8, 页码 587-598出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.exphem.2015.05.016
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资金
- NCI NIH HHS [T32 CA117846] Funding Source: Medline
- NHLBI NIH HHS [R01 HL114582, R01 HL111103] Funding Source: Medline
- NIDDK NIH HHS [R01 DK102759] Funding Source: Medline
- NIGMS NIH HHS [T32 GM063483] Funding Source: Medline
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 (C) 2015 ISEH - International Society for Experimental Hematology. Published by Elsevier Inc.
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