Abstract
Myeloid-derived suppressor cells (MDSCs) are a group of immunosuppressive cells that play crucial roles in promoting tumor growth and protecting tumors from immune recognition in tumor-bearing mice and cancer patients. Recently, it has been shown that the metabolic activity of MDSCs plays an important role in the regulation of their inhibitory function, especially in the processes of tumor occurrence and development. The MDSC metabolism, such as glycolysis, fatty acid oxidation and amino acid metabolism, is rewired in the tumor microenvironment (TME), which enhances the immunosuppressive activity, resulting in effector T cell apoptosis and suppressive cell proliferation. Herein, we summarized the recent progress in the metabolic reprogramming and immunosuppressive function of MDSCs during tumorigenesis.
Highlights
Myeloid-derived suppressive cells (MDSCs), which were first discovered in the 1970s and identified and named in 2007, are a group of heterogeneous cells expanded through pathological activation from bone marrow-derived immature myeloid cells (IMCs) during autoimmune diseases, infections, cancer and graft vs. host disease (GVHD) [1,2,3]
Recent studies have shown that the lipid metabolism of tumor-infiltrating Myeloid-derived suppressor cells (MDSCs) (T-MDSCs) is transformed to increase fatty acid uptake and improve FAO, accompanied by an increase in mitochondrial mass, oxygen consumption rate (OCR) and expression of key FAO enzymes, including carnitine palmitoyltransferase 1 (CPT1), acyl CoA dehydrogenase (ACADM), peroxisome proliferator-activated receptor gamma coactivator
The upregulation of these enzymes on MDSCs is induced by TGF-β-mammalian target of rapamycin (mTOR)-HIF-1 signaling and has been reported in peripheral blood and tumor tissues from non-small cell lung cancer (NSCLC) patients [87]
Summary
Myeloid-derived suppressive cells (MDSCs), which were first discovered in the 1970s and identified and named in 2007, are a group of heterogeneous cells expanded through pathological activation from bone marrow-derived immature myeloid cells (IMCs) during autoimmune diseases, infections, cancer and graft vs. host disease (GVHD) [1,2,3]. (4) microenvironment, establishing a premetastatic the antitumor immune response by suppressing T cells and natural killer (NK) cells, niche (pMN) reducing for cancer cells implantation; (5) inducing tumor mesenchymal epithelial transition for promoting the generation of immunosuppressive cells, such as regulatory T cells (Tregs) and expansion; and (6) promoting regulatory. TME, tumor microenvironment; HPC, through the circulatory system to the tumor site, in which MDSCs exert immunosuppressive functions by hemopoietic progenitor cell; CMP, common myeloid progenitor; GMP, granulocyte-macrophage progenitor; MB, myeloblast; MDP, TME, monocyte/macrophage and dendritic cell HPC, precursor; MDSC, generating anti-inflammatory cytokines. Tumor microenvironment; hemopoietic progenitor myeloid-derived suppressor cell; TAM, tumor-associated macrophage; DC, dendritic cell; Treg, cell; CMP, common myeloid progenitor; GMP, granulocyte-macrophage progenitor; MB, myeloblast; regulatory T cell; Teff, effector T cell; IL-10, interleukin-10; PGE2, prostaglandin E2; TGFβ, MDP, monocyte/macrophage and beta; dendritic cell precursor; myeloid-derived transforming growth factor.
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