ArticleArthritis research & therapy2018
Expansion and activation of monocytic-myeloid-derived suppressor cell via STAT3/arginase-I signaling in patients with ankylosing spondylitis.
Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- The role of PD-1 and Tim-3 in regulating the suppressive activity of myeloid-derived suppressor cells in axial spondyloarthritis: association with clinical and laboratory parameters.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Review
- Myeloid-derived suppressor cells-induced exhaustion of CD8 + T-cell participates in rejection after liver transplantation.Cell death & disease · 2024Article
- Dual roles of myeloid-derived suppressor cells in various diseases: a review.Archives of pharmacal research · 2024Review
- CD_99 G1 neutrophils modulate osteogenic differentiation of mesenchymal stem cells in the pathological process of ankylosing spondylitis.Annals of the rheumatic diseases · 2024Article
- Innate-immune cell distribution in pediatric HIV patients and uninfected controls.Revista do Instituto de Medicina Tropical de Sao Paulo · 2024Article
- Role of innate immunological/inflammatory pathways in myelodysplastic syndromes and AML: a narrative review.Experimental hematology & oncology · 2023Review
- The role of myeloid derived suppressor cells in musculoskeletal disorders.Frontiers in immunology · 2023Review
- The downregulation of type I IFN signaling in G-MDSCs under tumor conditions promotes their development towards an immunosuppressive phenotype.Cell death & disease · 2022Article
- Epigenetic modifications in the accumulation and function of myeloid-derived suppressor cells.Frontiers in immunology · 2022Review
- Article
- TRAF6 Regulates the Immunosuppressive Effects of Myeloid-Derived Suppressor Cells in Tumor-Bearing Host.Frontiers in immunology · 2021Article
- Modulation of Immunosuppression by Oligonucleotide-Based Molecules and Small Molecules Targeting Myeloid-Derived Suppressor Cells.Biomolecules & therapeutics · 2020Review
- Azithromycin Affords Neuroprotection in Rat Undergone Transient Focal Cerebral Ischemia.Frontiers in neuroscience · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnkylosing spondylitis (AS) is a chronic inflammatory rheumatic disease. The dysregulated immune system plays an important role in the pathogenesis of AS. Myeloid-derived suppressor cells (MDSCs) play a key immunoregulatory role in autoimmune arthritis. The aim of this study was to clarify the underlying immunoregulatory mechanism of MDSCs in patients with AS.
methodsFlow cytometry was used to analyze the phenotype of MDSCs among peripheral blood mononuclear cells (PBMCs) from 46 patients with AS and 46 healthy control subjects. The correlation between MDSC frequency and the disease index of patients with AS was evaluated. A T cell proliferation experiment was used to evaluate the immunosuppressive function of MDSCs.
resultsPolymorphonuclear (PMN) and monocytic (M)-MDSCs were significantly elevated in the PBMCs of patients with AS, when compared with levels in healthy controls. Additionally, M-MDSC levels correlated positively with the clinical index of AS, including the Bath ankylosing spondylitis disease activity index (BASDAI) score, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels. M-MDSCs derived from patients with AS suppressed T cell responses, and this effect was dependent on the induction of arginase-I. Furthermore, AS-derived M-MDSCs showed high levels of phosphorylated STAT3. Stattic, a STAT3-specific inhibitor, and STAT3-targeted siRNA abrogated the immunosuppressive function of M-MDSCs. Inhibition of STAT3 signaling also resulted in decreased arginase-I activity.
conclusionsSTAT3/arginase-I signaling plays an important role in both the expansion and activation of M-MDSCs in patients with AS. This information may be beneficial in developing novel therapeutic strategies for preventing AS.
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