Monocyte-Derived Macrophages Are Impaired in Myelodysplastic SyndromeReportar como inadecuado

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Journal of Immunology Research - Volume 2016 2016, Article ID 5479013, 7 pages -

Research ArticleDepartment of Hematology, General Hospital, Tianjin Medical University, Tianjin 300052, China

Received 7 October 2016; Accepted 23 November 2016

Academic Editor: Andréia M. Cardoso

Copyright © 2016 Yu Han et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. The myelodysplastic syndrome MDS comprises a group of clonal hematopoietic stem cell diseases characterized by cytopenia, dysplasia in one or more of the major myeloid lineages, ineffective hematopoiesis, and increased risk of development of acute myeloid leukemia AML. Macrophages are innate immune cells that ingest and degrade abnormal cells, debris, and foreign material and orchestrate inflammatory processes. We analyzed the role of macrophages from MDS patients in vitro. Methods. Macrophages were induced from peripheral blood of patients with MDS via granulocyte macrophage colony-stimulating factor GM-CSF. Phagocytic capacity of macrophages was measured with carboxyfluorescein succinimidyl ester and fluorescent microspheres. CD206 and signal regulatory protein alpha SIRPα on macrophages were detected by flow cytometry. Inducible nitric oxide synthase iNOS was measured by ELISA method. Results. Compared with normal control group, the number of monocytes increased in MDS patients. However, the monocytes showed impaired ability to induce macrophages and the number of macrophages induced from MDS samples was lower. Further, we demonstrated that the ex vivo phagocytic function of macrophages from MDS patients was impaired and levels of reorganization receptors CD206 and SIRPα were lower. Levels of iNOS secreted by macrophages in MDS were increased. Conclusions. Monocyte-derived macrophages are impaired in myelodysplastic syndromes.

Autor: Yu Han, Huaquan Wang, and Zonghong Shao



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