Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Palmitoylation, a critical post-translational protein modification, remains poorly understood in immune-mediated kidney diseases. Emerging evidence suggests Th17 cell infiltration drives fibrosis progression in immune nephritis, but the upstream molecular switches controlling this process require elucidation. We aimed to investigate the role of palmitoylation in modulating TEAD4 activity and its impact on Th17 cell infiltration in immune nephritis, suggesting that inhibition of palmitoylation could serve as a "brake" mechanism to impede disease progression.
Th17 cell infiltration in renal clinical samples and murine models was investigated via ELISA, immunofluorescence, and histopathological analyses. Mechanistic insights were obtained via metabolomic and transcriptomic profiling, co-immunoprecipitation, acyl-biotinyl exchange, Click-iT and, dual-luciferase reporter experiments.
Clinical and murine analyses revealed Th17 infiltration intensity positively correlated with IgAN severity. Mechanistically, Th17 cells are recruited by CCL20, which is upregulated through the transcription factor TEAD4 in injured tubular epithelial cells under inflammatory conditions. Notably, TEAD4 activity is regulated by palmitoylation modification rather than changes in protein expression levels. Further analysis identified ZDHHC14 as the key palmitoyltransferase mediating TEAD4 palmitoylation, and ZDHHC14 is highly expressed in renal tissues of both IgAN patients and model mice. Knockdown of ZDHHC14 significantly reduced CCL20 expression and subsequent Th17 cell infiltration. In vivo therapeutic experiments demonstrated that administration of the ZDHHC inhibitor 2-BP effectively attenuated Th17 cell infiltration and renal interstitial fibrosis in IgAN mice, markedly delaying disease progression.
This study provides the first evidence of TEAD4 palmitoylation-mediated regulation in immune-mediated kidney, and proposes a novel strategy to modulate Th17-driven disorders, with broad implications for autoimmune and fibrotic diseases.
