ArticleCell death & disease2023
FcγRIIIA activation-mediated up-regulation of glycolysis alters MDSCs modulation in CD4
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Phloretin Modulates STING Ubiquitination Degradation to Restrain Dendritic Cell Overactivation and Alleviate Sjögren's Syndrome.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Glycolysis drives vascular hyperpermeability in acute lung injury via lactate-GPR81 axis in endothelial cells.Cell communication and signaling : CCS · 2026Article
- Myeloid-Derived Suppressor Cells in Inflammatory Arthritis.International journal of molecular sciences · 2026Review
- An exploratory study on the metagenomic and proteomic characterization of hypothyroidism in the first half of pregnancy and correlation with Th1/Th2 balance.Frontiers in immunology · 2025Article
- Immunometabolic alteration of CD4Clinical and experimental medicine · 2024Article
- Exploring the Potential of Glycolytic Modulation in Myeloid-Derived Suppressor Cells for Immunotherapy and Disease Management.Immune network · 2024Review
- Emerging Role and Mechanism of Mesenchymal Stem Cells-Derived Extracellular Vesicles in Rheumatic Disease.Journal of inflammation research · 2024Review
- Modulation of myeloid-derived suppressor cell functions by oral inflammatory diseases and important oral pathogens.Frontiers in immunology · 2024Review
- Oxymatrine Alleviates Collagen-Induced Arthritis in Mice by Regulating the Immune Balance of T Cells.Molecules (Basel, Switzerland) · 2023Article
- New insights into the functions of MDSCs in autoimmune pathogenesis.Cellular & molecular immunology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our and other researchers' previous studies found that myeloid-derived suppressor cells (MDSCs) were increased, and these MDSCs, supposed to play immunosuppressive roles, showed significant pro-inflammatory effects in Sjögren's syndrome (SS). However, the key factors and potential mechanisms leading MDSCs to be inflammatory remain unclear. In this study, we found that MDSCs from SS patients were positively correlated with the percentages of Th17 cells, disease activity and serum autoantibodies, and showed higher levels of Fc gamma receptor (FcγR) IIIA and glycolysis. Most importantly, SS MDSCs or heat-aggregated IgG (HAIG)-treated MDSCs down-regulated Th1/Th2 ratio and up-regulated Th17/Treg ratio, which could be obviously rescued by IgG monomer or glycolysis inhibitor 2-DG. As well, the levels of FcγRIV and glycolysis in MDSCs and the ratio of Th17/Treg were increased, and the ratio of Th1/Th2 was decreased in SS-like NOD mice. Our study indicated that MDSCs showed pro-inflammatory phenotypes by disturbing CD4
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