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X. Zhu et al.
associated with MSC function via the regulation of IL-1β synthesis. Expectedly, ATRA inhibited IL-1β mRNA expression in MSC via upregulation of promoter DNA methylation. Further studies are warranted to confirm these data in a larger group of patients with primary ITP.
In conclusion, we have shown that enhanced comple- ment activation and the associated pro-inflammatory cytokine IL-1β could induce dysfunction of bone marrow MSC in ITP and consequently cause dynamic changes in niche CXCL12 and alterations in the location of megakaryocytes in the bone marrow. ATRA is a promis- ing therapeutic approach for repairing MSC dysfunction in primary ITP patients. The present study sheds light on complement activation in the pathogenesis of ITP and
provides new shreds of evidence confirming the general applicability of ATRA in the treatment of ITP.
Acknowledgments
This work was supported by the National Natural Science Foundation of China (n. 81470343 and n. 81670116), a Key Program of the National Natural Science Foundation of China (n. 81730004), the Beijing Natural Science Foundation (n. 7171013), the Beijing Municipal Science and Technology Commission (n. Z171100001017084), the National Key Research and Development Program of China (n. 2017YFA0105500 and n. 2017YFA0105503) and the Foundation for Innovation Research Groups of the National Natural Science Foundation of China (n. 81621001).
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