Figure S1. Graphical abstract of Plasmodium modulation of MDSC- and Treg-mediated regulation of CD8+ T cells in the tumor microenvironment. Tumor cytokines and chemokines inhibit the differentiation of myeloid cells in the tumor microenvironment, leading to the accumulation of MDSCs. The binding of cytokines to their receptors on MDSCs triggers the phosphorylation of several signal transduction molecules and the activation of transcription, resulting in the expression of downstream proteins. MDSCs express arginase 1, ROS, and iNOS, which inhibit cytotoxic T lymphocytes. The expression of anti-apoptosis proteins, Survivin and S100A9 enables MDSC proliferation and accumulation. Tumor-secreted cytokines convert naïve CD4+ T cells to Tregs in the tumor microenvironment. Tregs further inhibit CTLs by releasing molecules such as IL-10 and TGF-β. (G, cytokines; GR, cytokine receptors). Plasmodium infection inhibits tumor-derived cytokine and chemokine secretion in the tumor microenvironment, thereby inhibiting the conversion of myeloid cells to MDSCs, the expression of downstream proteins, the conversion of naïve CD4+ T cells to Tregs, and the expression of PD-1 on cytotoxic T cells. (TIF 1593 kb)