Tumor Immune Evasion Induced by Dysregulation of Erythroid Progenitor Cells Development

Cancer cells harness normal cells to facilitate tumor growth and metastasis. Within this complex network of interactions, the establishment and maintenance of immune evasion mechanisms are crucial for cancer progression. The escape from the immune surveillance results from multiple independent mecha...

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Bibliographic Details
Published in:Cancers 2021-02, Vol.13 (4), p.870
Main Authors: Grzywa, Tomasz M, Justyniarska, Magdalena, Nowis, Dominika, Golab, Jakub
Format: Article
Language:English
Subjects:
Apoptosis
Cancer
Cell differentiation
Cyclin-dependent kinases
Erythrocytes
Erythroid cells
Erythropoiesis
Fibroblasts
Growth factors
Homeostasis
Hypoxia
Immune evasion
Immune response
Immunosuppression
Immunosurveillance
Immunotherapy
Interleukin 10
Kinases
Lymphocytes T
Macrophages
Metastases
PD-L1 protein
Progenitor cells
Reactive oxygen species
Review
Spleen
Stem cells
Suppressor cells
Transforming growth factor-b
Tumor necrosis factor-TNF
Tumors
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Summary:Cancer cells harness normal cells to facilitate tumor growth and metastasis. Within this complex network of interactions, the establishment and maintenance of immune evasion mechanisms are crucial for cancer progression. The escape from the immune surveillance results from multiple independent mechanisms. Recent studies revealed that besides well-described myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs) or regulatory T-cells (Tregs), erythroid progenitor cells (EPCs) play an important role in the regulation of immune response and tumor progression. EPCs are immature erythroid cells that differentiate into oxygen-transporting red blood cells. They expand in the extramedullary sites, including the spleen, as well as infiltrate tumors. EPCs in cancer produce reactive oxygen species (ROS), transforming growth factor β (TGF-β), interleukin-10 (IL-10) and express programmed death-ligand 1 (PD-L1) and potently suppress T-cells. Thus, EPCs regulate antitumor, antiviral, and antimicrobial immunity, leading to immune suppression. Moreover, EPCs promote tumor growth by the secretion of growth factors, including artemin. The expansion of EPCs in cancer is an effect of the dysregulation of erythropoiesis, leading to the differentiation arrest and enrichment of early-stage EPCs. Therefore, anemia treatment, targeting ineffective erythropoiesis, and the promotion of EPC differentiation are promising strategies to reduce cancer-induced immunosuppression and the tumor-promoting effects of EPCs.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers13040870