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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.
CARD9, encoding an adaptor protein crucial for pathogen defense and gut mucosal immunity, was identified as a susceptibility gene for IgA nephropathy (IgAN) in previous GWAS. This study aimed to investigate the associations of CARD9 variants with IgAN and their potential functional implications in disease pathogenesis.
A total of 3,319 IgAN patients and 6,747 healthy controls were enrolled across three independent cohorts, and 10 candidate single-nucleotide polymorphisms were genotyped. Serum cytokines and galactose-deficient IgA1 (Gd-IgA1) were measured by Luminex technology and ELISA, respectively. Molecular dynamics (MD) simulations assessed the residue mutations and dynamic properties of the CARD9 protein. Expression profiling data from the GEO database were used to explore CARD9 expression and relevant pathways in renal tissues of IgAN patients. We also examined the association of CARD9 variant and alterations in the gut microbiota using our previously published 16S rRNA sequencing data.
We found that rs4077515-T (S12N mutation) was associated with increased IgAN risk (OR = 1.26, 95% CI = 1.07–1.49, P = 0.006) and greater disease severity. The S12N mutation was significantly correlated with elevated serum levels of Gd-IgA1 and multiple cytokines particularly IL-17, IL-6, IL-1β, IL-8, and TNF-α. MD simulations revealed that the S12N mutation induced conformational changes in CARD9, reduced its structural stability and affinity for BCL10, and remodeled the binding interface. Gene expression profiling data suggested CARD9 expression was upregulated in the renal interstitium of IgAN patients and was linked to Dectin-1, NF-κB signaling and B cell-related immune pathways. Interestingly, IgAN patients carrying the S12N mutation not only exhibited a significantly higher abundance of Candidatus Stoquefichus and a reduced abundance of Collinsella and Gordonibacter, but also showed differences in microbial community composition as revealed by beta diversity analysis.
Our results suggest that CARD9 S12N mutation confers susceptibility to IgAN, potentially by modulating the CARD9-mediated immune responses.
