Abstract
Over the past decade, cancer immunotherapy has been steering immune responses toward cancer cell eradication. However, these immunotherapeutic approaches are hampered by the tumor-promoting nature of myeloid cells, including monocytes, macrophages, and neutrophils. Despite the arsenal of defense strategies against foreign invaders, myeloid cells succumb to the instructions of an established tumor. Interestingly, the most primordial defense responses employed by myeloid cells against pathogens, such as complement activation, antibody-dependent cell cytotoxicity and phagocytosis, actually seem to favor cancer progression. In this review, we discuss how rudimentary defense mechanisms deployed by myeloid cells can promote tumor progression.
Highlights
Immune cells abundantly infiltrate tumors, creating a complex environment mediated by repetitive cycles of antitumor responses and immune evasion [1]
Myeloid Innate Responses in Tumors eosinophils [17], basophils [18] and mast cells [19], further research is required to fully elucidate their role in cancer, as antitumoral roles have been described [20, 21]. Another myeloid population in the tumor microenvironment (TME) are dendritic cells (DCs), that originate from different precursors and display various phenotypes, ranging from immunosuppressive monocyte-derived DCs (Mo-DCs) to immunocompetent cDC1 and cDC2 subsets [22]
The innate immune response by myeloid cells occurs as a succession of events starting at signaling through cytosolic or surface PRRs, followed by effector responses including the release of cytokines, reactive oxygen species (ROS), reactive nitrogen species (RNS), antibacterial peptides and degranulation (Figure 1)
Summary
Immune cells abundantly infiltrate tumors, creating a complex environment mediated by repetitive cycles of antitumor responses and immune evasion [1]. Myeloid Innate Responses in Tumors eosinophils [17], basophils [18] and mast cells [19], further research is required to fully elucidate their role in cancer, as antitumoral roles have been described [20, 21]. Another myeloid population in the tumor microenvironment (TME) are DCs, that originate from different precursors and display various phenotypes, ranging from immunosuppressive monocyte-derived DCs (Mo-DCs) to immunocompetent cDC1 and cDC2 subsets [22].
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