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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.
Minimal change disease (MCD) represents the predominant cause of steroid-dependent nephrotic syndrome. While rituximab (RTX) demonstrates clinical efficacy in steroid-dependent MCD through B cell depletion, the precise immunological mechanisms determining treatment responsiveness remain incompletely understood, particularly regarding secondary effects on T cell populations.
We conducted single-cell RNA sequencing and T cell receptor analysis on peripheral blood T cells from six adults with steroid-dependent MCD (three RTX responders, three non-responders) sampled pre-treatment and one month after RTX administration. In another cohort, reactive oxygen species (ROS) levels in each cell subset were assessed by flow cytometry. To contextualize our findings within broader immune networks, we performed comparative re-analysis of publicly available pediatric INS single-cell RNA sequencing datasets.
RTX responders demonstrated extensive transcriptomic reprogramming across T cell subsets, characterized by enhanced oxidative phosphorylation (OXPHOS) activity and coordinated metabolic recalibration in mature T cells. Notably, responders exhibited decreased ROS production concurrent with increased OXPHOS—a phenomenon explained by upregulation of ROS-coping pathways and downregulation of oxidative stress-associated genes. Non-responders showed minimal transcriptomic changes. RTX treatment in responders was associated with significant reduction in exhausted CD8⁺ T cell populations and clonal expansion of CD4⁺ cytotoxic T cells (CD4⁺ CTLs) with enhanced metabolic competence. In addition, re-analysis of public data of pediatric INS patients revealed aberrant B-T cell communication networks involving CD4⁺ CTLs.
RTX efficacy may extend beyond B cell depletion to encompass metabolic and functional restoration of T cell compartments. These findings suggest that T cell transcriptomic reprogramming may serve as predictive biomarkers for RTX responsiveness in steroid-dependent MCD, potentially informing personalized treatment strategies.
