ArticleEuropean journal of immunology2018
Arginase-1 is neither constitutively expressed in nor required for myeloid-derived suppressor cell-mediated inhibition of T-cell proliferation.
Article in European journal of immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
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- Identification of immunosuppressive neutrophils using multi-omics: why functional testing remains key.Frontiers in immunology · 2026Review
- From immune exclusion to exhaustion: tumor microenvironment drives therapy response.Frontiers in immunology · 2026Review
- Targeting MDSCs in cancer: emerging immunotherapeutic and metabolic strategies.Frontiers in immunology · 2026Review
- Metabolic checkpoints in immune cell reprogramming: rewiring immunometabolism for cancer therapy.Molecular cancer · 2025Review
- Arginine metabolism in myeloid cells in health and disease.Seminars in immunopathology · 2025Review
- Interactions between glioblastoma and myeloid cells.Frontiers in cell and developmental biology · 2025Review
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- VISTA promotes the metabolism and differentiation of myeloid-derived suppressor cells by STAT3 and polyamine-dependent mechanisms.Cell reports · 2024Article
- Target delivery of a PD-1-TREM2 scFv by CAR-T cells enhances anti-tumor efficacy in colorectal cancer.Molecular cancer · 2023Article
- Amino acid metabolism in immune cells: essential regulators of the effector functions, and promising opportunities to enhance cancer immunotherapy.Journal of hematology & oncology · 2023Review
- Immunosuppressive cells in oncolytic virotherapy for glioma: challenges and solutions.Frontiers in cellular and infection microbiology · 2023Review
- Reprogramming of sentinel lymph node microenvironment during tumor metastasis.Journal of biomedical science · 2022Review
- Murine myeloid derived suppressor cells possess a range of suppressive mechanisms-Granzyme B is not among them.Cancer immunology, immunotherapy : CII · 2022Article
- Myeloid-derived suppressor cells in hematologic malignancies: two sides of the same coin.Experimental hematology & oncology · 2022Review
- Induction of M-MDSCs with IL6/GM-CSF from adherence monocytes and inhibition by WP1066.Experimental and therapeutic medicine · 2022Article
- Role of myeloid-derived suppressor cells in the formation of pre-metastatic niche.Frontiers in oncology · 2022Review
- Myeloid-Derived Suppressor Cells Mediate T Cell Dysfunction in Nonhuman Primate TB Granulomas.mBio · 2021Article
- Age-related expansion and increased osteoclastogenic potential of myeloid-derived suppressor cells.Molecular immunology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Although previous reports suggest that tumor-induced myeloid-derived suppressor cells (MDSC) inhibit T cells by L-arginine depletion through arginase-1 activity, we herein show that arginase-1 is neither inherently expressed in MDSC nor required for MDSC-mediated inhibition. Employing Percoll density gradients, large expansions of MDSC in the bone marrow of tumor-bearing mice were isolated and demonstrated potent inhibition in T-cell proliferation activated by TCR-ligation, Concanavalin A, PMA plus ionomycin, or IL-2. Despite demonstrating characteristic immunosuppressive capacity, these MDSC exhibit no arginase-1 expression and/or exert their inhibitory effects independent of arginase-1 activity. However, arginase-1 expression in MDSC can be induced by exposure to TCR-activated T cells or their culture medium, but not T cells activated by other means or growing tumor cells. Further investigation reveals multiple cytokines secreted by TCR-activated T cells as orchestrating two signaling-relay axes, IL-6-to-IL-4 and GM-CSF/IL-4-to-IL-10, leading to arginase-1 expression in MDSC. Specifically, IL-6 signaling increases IL-4R, enabling IL-4 to induce arginase-1 expression; similarly, GM-CSF in concert with IL-4 induces IL-10R, allowing IL-10-mediated induction. Surprisingly, our study indicates that induction of arginase-1 expression is not conducive to the critical MDSC-mediated inhibition toward T cells, which is rather dependent on direct cell contacts undiminished by PD-L1 blockade or SIRPα deficiency.
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