Published November 2021 | Version v1
Journal article

Characteristics of macrophages from myelodysplastic syndrome microenvironment

  • 1. Department of Hematology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006 (China)

Description

Highlights: • MDS macrophages exhibited more M2-related characteristics. • Ferric chloride polarized MDS macrophages to exhibit more M1-related characteristics. • DFO partially reversed the M1-related characteristics induced by ferric chloride. Myelodysplastic syndrome (MDS) is a heterogeneous group of clonal hematopoietic neoplasms. The progression of malignancy is closely associated with immune regulation. Macrophages are indispensable tissue components and have been proposed to play a role in the pathophysiology of hematopoietic malignancies. However, the specific role of macrophages in the development of MDS remains unclear. Here, we investigated the characteristics and phenotypic evolution of macrophages from patients with MDS. Macrophages from patients with MDS expressed CD68, CD86 and CD163. Furthermore, MDS macrophages exhibited more M2-related characteristics. Moreover, a number of phenotype-associated genes in MDS macrophages exhibited diverse responses to iron overload or iron chelation upon stimulation by ferric chloride or deferoxamine (DFO, an iron chelator). Ferric chloride polarized MDS macrophages to exhibit more M1-related characteristics, a phenomenon that could be partially reversed by DFO. Therefore, this study reveals the characteristics and phenotypic evolution of MDS macrophages and broadens the knowledge of macrophage plasticity in hematopoietic malignancies.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.yexcr.2021.112837

Additional details

Identifiers

DOI
10.1016/j.yexcr.2021.112837;
PII
S0014482721003918;

Publishing Information

Journal Title
Experimental Cell Research
Journal Volume
408
Journal Issue
1
Journal Page Range
vp.
ISSN
0014-4827
CODEN
ECREAL

Optional Information

Copyright
Copyright (c) 2021 Elsevier Inc. All rights reserved.