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.
IgA nephropathy (IgAN) is a chronic, immune-mediated kidney disorder characterized by gut-derived renal deposition of galactose-deficient IgA1 antibodies in the glomeruli of the kidney. Peyer’s patches (PPs) in the distal ileum serve as key sites for B-cell priming, IgA class switching, and mucosal immunity. Budesonide, the active substance of nefecon (an FDA-approved targeted-release budesonide formulation), has demonstrated B-cell suppressive effects, yet its tissue-specific immunomodulatory role in PPs remains incompletely defined. The objective of this study was to investigate the immunological impact of orally administered budesonide on B- and T-cell subsets in murine PPs following in vivo stimulation with R848, a TLR7/8 agonist that activates mucosal immunity.
Female Balb/c mice were randomized into four treatment groups: vehicle (10% dimethyl sulfoxide in phosphate-buffered saline), R848 alone, budesonide alone, and R848 + budesonide. Budesonide (3 mg/kg) was administered orally at 6 and 24 hours post-intraperitoneal R848 injection. Mice were sacrificed at 28, 48, 72, 96, and 168 hours post-treatment. PPs were harvested for flow cytometric analysis of B- and T-cell subsets, activation markers (CD69, CD25, CD86), proliferation (Ki67), cytokine production (interferon [IFN]-γ, interleukin [IL]-10), and apoptosis (cleaved caspase-3). Ex vivo stimulation with R848 (500 ng/mL) was performed for 72 hours to assess cell viability and phenotype.
The R848 + budesonide group showed reduced total PP cell counts (Figure) and increased apoptosis (cleaved caspase-3+ cells). Significant reductions were observed in CD19+ B cells, IgA+ and IgG+, IgD− subsets, germinal center B cells (GL7+, CD95+), and plasma blasts (CD138+), with transient increases in IgA+ plasma cells at 48 and 72 hours. T-cell analysis revealed decreased CD3+ counts and elevated proportions of activated (CD69+, CD25+), costimulatory (CD86+), proliferating (Ki67+), and regulatory (FOXP3+) T cells. IL-10+ and IFN-γ+ Tregs were reduced, indicating a shift in regulatory balance. Early B-cell activation (CD69+, CD25−) increased, while Ki67+ B-cell proliferation declined over time. Ex vivo stimulation showed poor viability (2–20%) but mirrored in vivo trends.
Budesonide, particularly following stimulation by R848, exerts robust immunomodulatory effects in PPs by suppressing B-cell populations involved in IgA production and altering T-cell activation. To our knowledge, this is the first time a study has shown apoptotic cells within the PPs after oral treatment with budesonide. These findings support the localized action of nefecon for the treatment of IgAN. Further studies using transcriptomic profiling and disease models are warranted to elucidate budesonide’s immunological mechanisms in PPs.
