2017
DOI: 10.1016/j.exphem.2017.06.143
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Altered HSC fate underlies aberrant blood phenotypes in rheumatoid arthritis

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“…In ulcerative colitis, the enhanced serum levels of IFN-γ in patients are highly associated with the development of clonal haematopoiesis, especially with DNMT3A and PPM1D mutations [89]. The systemic increase in IL-1 and TNF in rheumatoid arthritis promotes myeloid-biased differentiation in HSCs, along with broad suppression on diverse HSC-niche cell types [90,91] Hematologic malignancies: continuous dysregulated inflammatory stress on HSCs may contribute to the emergence of mutations and confer selective advantages to certain HSC clones, promoting clonal haematopoiesis. Functional loss of TET2, an epigenetic regulator, is a common mutation in myeloid malignancies and promotes haematopoietic transformation by elevating the self-renewal capacity of the mutated cells [92,93].…”
Section: Chronic Inflammationmentioning
confidence: 99%
“…In ulcerative colitis, the enhanced serum levels of IFN-γ in patients are highly associated with the development of clonal haematopoiesis, especially with DNMT3A and PPM1D mutations [89]. The systemic increase in IL-1 and TNF in rheumatoid arthritis promotes myeloid-biased differentiation in HSCs, along with broad suppression on diverse HSC-niche cell types [90,91] Hematologic malignancies: continuous dysregulated inflammatory stress on HSCs may contribute to the emergence of mutations and confer selective advantages to certain HSC clones, promoting clonal haematopoiesis. Functional loss of TET2, an epigenetic regulator, is a common mutation in myeloid malignancies and promotes haematopoietic transformation by elevating the self-renewal capacity of the mutated cells [92,93].…”
Section: Chronic Inflammationmentioning
confidence: 99%