Abstract
Myeloid malignancies arise from an altered hematopoietic stem cell and mainly comprise acute myeloid leukemia, myelodysplastic syndromes, myeloproliferative malignancies, and chronic myelomonocytic leukemia. Myeloid neoplastic leukemic cells may influence the growth and differentiation of other hematopoietic cell lineages in peripheral blood and bone marrow. Myeloid-derived suppressor cells (MDSCs) and mesenchymal stromal cells (MSCs) display immunoregulatory properties by controlling the innate and adaptive immune systems that may induce a tolerant and supportive microenvironment for neoplasm development. This review analyzes the main features of MDSCs and MSCs in myeloid malignancies. The number of MDSCs is elevated in myeloid malignancies exhibiting high immunosuppressive capacities, whereas MSCs, in addition to their immunosuppression contribution, regulate myeloid leukemia cell proliferation, apoptosis, and chemotherapy resistance. Moreover, MSCs may promote MDSC expansion, which may mutually contribute to the creation of an immuno-tolerant neoplasm microenvironment. Understanding the implication of MDSCs and MSCs in myeloid malignancies may favor their potential use in immunotherapeutic strategies.
Highlights
Med. 2021, 10, 2788 the International Society for Cellular Therapy (ISCT), in 2006, as follows: mesenchymal stem cells (MSCs) must be plastic-adherent when maintained under standard culture conditions; more than 95% of cells in a given population of MSCs should express CD90, CD73, and CD105 and lack the expression of CD45, CD34, CD14 or CD11b, CD79α, or CD19, and human leukocyte antigen (HLA) class II surface molecules; and MSCs must differentiate into osteoblasts, adipocytes, and chondroblasts under standard conditions in vitro [25,26]
Myeloid-derived suppressor cells (MDSCs) may induce the suppression of T-cell activation and apoptosis through cell–cell interaction mediated by immune checkpoint proteins, such as the programmed death-1 (PD-1) molecule with its cognate ligands PD-L1 and PD-L2 [60]
It is necessary to conduct new investigations addressing the mutual collaboration of MSCs and MDSCs in these groups of hematopoietic stem cell disorders, which may improve the understanding of microenvironment roles in the etiology of Ph- myeloproliferative neoplasms (MPNs) malignancies
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Through cell-intrinsic HSC characteristics and extrinsic signals, the BM microenvironment finely controls blood production, and BM niche perturbations contribute to the emergence of hematopoietic malignancies. Patients with myeloid malignancies display increased numbers of MDSCs in peripheral blood (PB) and BM and, due to their immunomodulatory function, may contribute to the escape of neoplastic cells from immunosurveillance, which appears to play a crucial role in maintaining the immune suppression within the tumor niche [5,6,7]. MSCs contribute to the progression of myeloid malignancies by establishing a favorable tumor microenvironment and displaying immunomodulatory properties by inhibiting the proliferation and function of immune cells, which contribute significantly to the pathogenesis of myeloid malignancies [10]. This review provides perspectives on new strategies being used to improve current therapies, which may ameliorate cancer management strategies to improve the life expectancy of patients diagnosed with myeloid malignancies
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