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. Author manuscript; available in PMC: 2023 Aug 1.
Published in final edited form as: Trends Pharmacol Sci. 2022 May 7;43(8):686–700. doi: 10.1016/j.tips.2022.04.002

Figure 2. Pharmacological tools to target the GBM–MDSC symbiosisw.

Figure 2.

GBM cell-derived ligands, exosomes, and cytokines recruit and activate MDSCs, which, in turn, inhibit T cell proliferation and function and promote GBM tumor growth. Pharmacological approaches targeting MDSC infiltration and activation during the GBM–MDSC symbiosis are proposed. The key targets and associated drug candidates are indicated. Sexual dimorphism of MDSCs also appears to be a target for GBM therapy: low dose of chemotherapy (fludarabine and capecitabine) inhibits M-MDSC proliferation in male GBM. By contrast, anti-IL-1β treatment inhibits PMN-MDSC function and enhances CD8+ T cell-mediated antitumor immunity in female GBM. Abbreviations: 2-ME2, 2-Methoxyestradiol; CCL2, C-C motif chemokine ligand 2; CCR2/4, C-C motif chemokine receptor 2/4; CLXCL1/2, C-X-C motif ligand 1/2; DUSP3, dual specificity phosphatase 3; ERK, extracellular signal-regulated kinase, GAMs, glioma-associated macrophages and microglia; GBM, glioblastoma; IL-1β/R, interleukin-1β/receptor; INFγ, interferon gamma; MIF, macrophage migration inhibitory factor; M-MDSCs, monocytic myeloid-derived suppressor cells; OPG, osteoprotegerin, PMN-MDSC, polymorphonuclear myeloid-derived suppressor cells.