Abstract
Tumor-mediated regulation of the host immune system involves an intricate signaling network that results in the tumor's inherent survival benefit. Myeloid cells are central in orchestrating the mechanisms by which tumors escape immune detection and continue their proliferative programming. Myeloid cell activation has historically been classified using a dichotomous system of classical (M1-like) and alternative (M2-like) states, defining general pro- and anti-inflammatory functions, respectively. Explosions in bioinformatics analyses have rapidly expanded the definitions of myeloid cell pro- and anti-inflammatory states with different combinations of tissue- and disease-specific phenotypic and functional markers. These new definitions have allowed researchers to target specific subsets of disease-propagating myeloid cells in order to modify or arrest the natural progression of the associated disease, especially in the context of tumor-immune interactions. Here, we discuss the myeloid cell contribution to solid tumor initiation and maintenance, and strategies to reprogram their phenotypic and functional fate, thereby disabling the network that benefits tumor survival.
Highlights
In recent decades the traditional view of tumor development and metastasis has evolved to include new and emerging cell types, extrinsic to the tumor itself
Over time it has become apparent that tumors are composed of many cell types from different origins, all with varying functions
When the tumor microenvironment being discussed relates to the influx and function of the immune system, it is termed the tumor immune microenvironment (TIME) [2]
Summary
In recent decades the traditional view of tumor development and metastasis has evolved to include new and emerging cell types, extrinsic to the tumor itself. Two central groups of suppressive myeloid cells are the tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) [6]. Despite established knowledge that TAM/MDSC infiltration is associated with worse prognosis [93], it is clear that not all myeloid cells in the tumor microenvironment directly benefit the growing malignancy.
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