Abstract
Simple SummaryIn this review, we summarize the effects of various cytokines and chemokines as a network to regulate the expansion, recruitment, and immunosuppressive functions of myeloid-derived suppressor cells in cancer metastasis.Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells that impair immune cell functions and promote tumor progression. Mounting evidence indicates that cytokines and chemokines in the tumor microenvironment alter MDSCs. Various cytokines and chemokines are involved in MDSC production, their infiltration into tumors, and their exertion of suppressive functions. Here, we consider those cytokines, chemokines, and MDSCs as an intricately connected, complex system and we focus on how tumors manipulate the MDSCs through various cytokines and chemokines. We also discuss treatment capitalizing on cytokines/chemokine signaling aimed at combating the potent immunosuppressive activities of MDSCs to improve disease outcomes.
Highlights
Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells derived from bone marrow progenitor cells with potent suppression of antitumor immunity to support tumor progression
MDSCs migrated into tumor microenvironment (TME) are dominantly monocytic MDSCs (M-MDSCs) with enhanced suppressive phenotypes that rapidly differentiate into tumor-associated macrophages [2]
We present a comprehensive overview of individual cytokine- and chemokine-signaling targeting MDSCs in TME
Summary
Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells derived from bone marrow progenitor cells with potent suppression of antitumor immunity to support tumor progression. Elevated levels of MDSCs in the peripheral blood and tumor microenvironment (TME) have been correlated with cancer progression. MDSCs in peripheral lymphoid organs and blood are mostly PMN-MDSCs with modest suppressive activity and that differentiate into macrophages and dendritic cells. MDSCs migrated into TME are dominantly M-MDSCs with enhanced suppressive phenotypes that rapidly differentiate into tumor-associated macrophages [2]. The nature of immune suppression by MDSCs is to hamper the recognition of tumor cells by cytotoxic T lymphocytes in non-specific ways through ROS, Arg-1, NO, and peroxynitrite (PNT), and in an antigen-specific way. Most studies examined individual cytokines and chemokines independently, which produced fragmented information and led to a convoluted view of their role in MDSC functions in cancer. We present a comprehensive overview of individual cytokine- and chemokine-signaling targeting MDSCs in TME.
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