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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
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Interferon-inducible protein 16 (IFI16), a member of the interferon-inducible p200 protein family, is involved in inflammasome assembly and the activation of interferon gene pathways. Recent studies have indicated that IFI16 participates in autoimmune responses such as systemic lupus erythematosus (SLE), Sjögren's syndrome, and rheumatoid arthritis. However, the expression and significance of IFI16 in primary glomerular diseases including IgA nephropathy (IgAN) remain unclear at present. Therefore, this study aimed to investigate IFI16 expression in the renal tissues and peripheral blood of IgAN patients, and further analyze its correlation with pathological, clinical severity and prognosis.
1. A total of 52 IgAN patients and 8 healthy controls were enrolled in this study. Renal tissue sections were subjected to immunohistochemical staining for IFI16, followed by semi-quantitative analysis.
2. Multiplex immunofluorescence staining were performed on renal pathological specimens to examine the co-localization of IFI16 with glomerular parenchymal cells and interstitial inflammatory cells.
3. qPCR was used to detect IFI16 expression in peripheral blood mononuclear cells (PBMCs).
4. Flow cytometry was employed to measure nuclear expression of IFI16 in T cells, B cells, and monocyte-macrophages.
5. Correlations between IFI16 expression (in both peripheral blood and renal tissues) and clinical parameters, pathological severity were analyzed.
6. After 3 years of treatment for IgA nephropathy patients (including RASi, glucocorticoids, or telitacicept, etc.), an analysis of the proportion of eGFR decline by 30% in the IFI16 high-expression group and the IFI16 low-expression group.
1. Significant nuclear expression of IFI16 was observed in both glomeruli and renal tubulointerstitium of IgAN patients, which was markedly higher than that in healthy controls.
2. Multiplex immunofluorescence staining revealed distrink co-localization of IFI16 with podocytes and capillary endothelial cells in the glomeruli, but no location was found with mesangial cells. Additionally, no co-localization was detected with proximal renal tubules. Notably, IFI16 showed definite co-localization with inflammatory cells (including T cells, B cells, macrophages, and neutrophils) in glomeruli and renal interstitium.
3. In the Lee grading system, IFI16 expression in grade IV IgAN patients was higher than in grades II, III, and V. According to the Oxford MEST-C classification, IFI16 expression was higher in M1 than in M0 glomeruli, higher in E1 than in E0, and higher in T1–T2 than in T0 renal interstitium. No significant differences were observed between S0 and S1 or among C0, C1, and C2. Additionally, IFI16 expression was higher in glomeruli with inflammatory cell infiltration than in those without.
4. In IgAN patients, IFI16 expression levels in both glomeruli and renal interstitium were positively correlated with proteinuria, but not with urinary red blood cell count. Specifically, interstitial IFI16 expression was positively correlated with serum creatinine levels and negatively correlated with eGFR.
5. In PBMCs of IgAN patients, IFI16 was expressed in the nuclei of monocyte-macrophages, T cells, and B cells. Further analysis showed that IFI16 expression in PBMCs was significantly higher in IgAN patients than in healthy controls. Moreover, patients with urinary protein >0.75 g/d had higher IFI16 expression in PBMCs than those with ≤0.75 g/d. In the Lee grading system, grade IV patients exhibited higher IFI16 expression in PBMCs than grade III and V patients.
6. Multivariate Cox hazard analysis of Prognosis indicated that high IFI16 expression in glomeruli is an independent risk factor for eGFR decline in IgAN patients.
1. IFI16 is expressed in the nuclei of peripheral blood leukocytes and renal cells—including podocytes, endothelial cells, and inflammatory cells—in IgAN patients.
2. IFI16 expression in both peripheral blood PBMCs and renal tissues is significantly elevated in IgAN patients compared to healthy controls.
3. IFI16 expression is closely associated with renal pathological and clinical severity in IgAN patients, and increased renal IFI16 expression is strongly correlated with poor prognosis.
