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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerular disease. Recent studies suggest that Th17 cell-mediated inflammation is a key pathogenic factor in IgAN. Myeloid-derived suppressor cells (MDSCs), a population of immature myeloid progenitor cells originating from the bone marrow, have recently been implicated in immune responses across multiple autoimmune diseases. However, the expression and specific role of MDSCs in IgAN remain unclear. This study aims to investigate the expression of myeloid-derived suppressor cells and their subtypes in IgA nephropathy, along with their pro-Th17 effects, and to elucidate the mechanisms underlying these effects. This research may provide novel insights for treating immune-inflammatory diseases, particularly IgA nephropathy.
(1) The study subjects comprised 20 patients with IgA nephropathy confirmed by renal biopsy and 20 healthy controls from the Nephrology Department of the First Hospital of Jilin University. Exclusion criteria included concurrent severe infection, history of malignant tumors, and concomitant autoimmune diseases. Participants enrolled after signing informed consent forms.
(2) Four milliliters of peripheral blood were collected from each group. Mononuclear cells were isolated and analyzed via flow cytometry staining for CD11b/HLA-DR/CD33/CD14/CD66. Peripheral blood mononuclear cells were analyzed by flow cytometry to determine the proportions of MDSCs (CD11b+HLADR-CD33+) and their subsets: monocyte-derived (M)-MDSCs (CD11b+HLADR-CD33+CD14+) and granulocyte-derived (G)-MDSCs (CD11b+HLADR-CD33+CD66B+).
(3) Isolate peripheral blood mononuclear cells, add PMA (300 ng/ml), ionomycin (1 µg/ml), and BFA (1 µg/ml), incubate in a CO₂ incubator for 6 hours, perform intracellular flow cytometry staining for CD4/IL17A/IL17F, and use flow cytometry to determine the proportion of Th17 cells (CD4+IL17A+ and CD4+IL17F+) in peripheral blood from IgA nephropathy patients and healthy controls; measure IL-17A and IL-17F expression in serum from both groups using ELISA. Immunofluorescence staining was used to visualize IL-17 deposition in glomeruli of renal biopsy specimens from IgA patients. Hematoxylin-eosin staining and Schiff's periodic acid staining were employed to examine pathological alterations in renal tissues from IgA nephropathy lesions.
(4) Measure serum arginase-1 (Arg-1) activity in IgA nephropathy patients and healthy controls, comparing Arg-1 activity changes between groups. Perform intracellular flow cytometry staining for CD11b/HLA-DR/CD33/CD14/CD66/Arg-1. Utilize flow cytometric analysis to detect Arg-1 expression in myeloid-derived suppressor cells (MDSCs) from IgA nephropathy patients and healthy controls. Compare similarities and differences in Arg-1 expression between MDSCs and their subsets derived from IgA patients versus healthy controls.
(5) Peripheral blood naive CD4+ T cells from IgA nephropathy patients, sorted by magnetic bead separation, were cultured under in vitro Th17 polarization conditions (TGF-β 5ng/ml, IL-6 20ng/ml, anti-CD28-mAb 1μg/ml, IL-1β 10ng/ml, IL-23 10 ng/ml, anti-IFN-γ mAb 5 µg/ml, anti-IL-4 mAb 5 μg/ml) and supplemented with flow-sorted MDSCs and/or the arginine-1 inhibitor nor-NOHA (300 μM). After 6–7 days of culture, the proportion of Th17 cells and IL-17 levels in the supernatant were assessed to determine the pro-Th17 differentiation effect of MDSCs and its molecular mechanisms.
(1) Compared with healthy controls, the proportion and number of MDSCs and their subtypes in peripheral blood were significantly increased in patients with IgA nephropathy.
(2) Peripheral blood Th17 cell expression and serum IL-17A and IL-17F levels were markedly higher in IgA nephropathy patients than in healthy controls. Deposition of IL-17A and IL-17F along glomerular capillary walls was observed in affected renal tissue.
(3) MDSCs produce Arg-1, predominantly via the granulocyte subtype. The mean fluorescence intensity of Arg-1 in G-MDSCs from IgA nephropathy patients was enhanced compared to healthy controls. Concurrently, serum arginase activity was elevated in IgA nephropathy patients relative to healthy controls.
(4) In vitro Th17 polarization assays demonstrated that MDSCs significantly promoted Th17 cell differentiation, with increased IL-17 levels in culture supernatants. This pro-Th17 differentiation effect of MDSCs was Arg-1-dependent.
Our study provides direct evidence for the pathogenic role of MDSCs in IgA nephropathy, demonstrating that MDSCs are significantly expanded in peripheral blood of patients with IgA nephropathy. These cells exert pathogenic effects by secreting Arg-1, which promotes Th17 differentiation and IL-17 production. This suggests that MDSCs or Arg-1 may serve as novel therapeutic targets for IgA nephropathy and other Th17 cell-mediated immune inflammatory diseases.
