Tumor-induced myeloid deviation: when myeloid-derived suppressor cells meet tumor-associated macrophages

ZEB1‐regulated inflammatory phenotype in breast cancer cells

“…MDSCs comprise heterogeneous cell populations that have the potential for immunosuppressive activity. MDSCs induce immune tolerance in the tumor microenvironment by suppressing cytotoxic T‐lymphocyte activity (Gabrilovich et al ., 2012; Ugel et al ., 2015). They are defined as CD11b + Gr‐1 + cells in mouse and are categorized as polymorphonuclear (PMN)‐MDSCs and monocytic (Mo)‐MDSCs.…”

ILC2-modulated T cell–to-MDSC balance is associated with bladder cancer recurrence

“…This study highlights the crucial need to restrain the tumor-induced "immunosuppressive switch" (63) by targeting MDSCs to tilt the balance in favor of T cells. A number of compounds were found to target MDSCs (10,11). One of these compounds, doxorubicin, may be of interest, as it selectively targets monocytic MDSCs in humans (64).…”

“…Of note, while CD115 (CSF1-R) was upregulated following IL-13 treatment in both HLA-DR hi and HLA-DR lo cells, all other monocyte and macrophage surface markers tested showed lower expression, including that of the M2 marker CD163 (Supplemental Figure 7C). Therefore, it seems that the ability of IL-13 to induce suppressive function in monocytic cells is attributable to an induction of M-MDSCs rather than of M2 macrophages, although the differences between these subsets remain unclear (11). Furthermore, IL-13 transcriptionally upregulated ARG1, iNOS, and C/EBPβ (Supplemental Figure 7D), which were also found to be expressed in urine M-MDSCs from patients ( Figure 1, D and E).…”

“…We found that the ratio of T cells to monocytic myeloid-derived suppressor cells (M-MDSCs), known to dampen antitumor immunity (10,11), is strongly associated with recurrence-free survival outcomes. Of note, BCG treatment does not seem to alter this ratio.…”

Immune targets and neoantigens for cancer immunotherapy and precision medicine

“…These include checkpoints or roadblocks (cytotoxic T lymphocyte antigen-4 (CTLA-4), programmed cell death-1 (PD-1) and its ligand PD-L1) for T cell activation and function [24][25][26], regulatory T cells, other immunosuppressive cells and inhibitory cytokines [27][28][29][30][31][32][33]. To enhance antitumor immunity, it is necessary to remove these roadblocks so that T cells can be fully activated and functional for the eradication of cancer cells.…”