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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.
Although chronic antibody-mediated rejection (CAMR) and autoimmune diseases target distinct antigens originating from donors and from the self, their effector mechanisms may converge. We sought to elucidate shared and disease-specific immune programs across alloimmune and autoimmune contexts using large-scale single-cell transcriptomics.
We generated an integrated atlas of more than 450,000 cells from peripheral blood and renal biopsies of CAMR, SAF, and healthy controls, combined with 3.1 million immune cells from 659 peripheral-blood samples encompassing autoimmune, inflammatory, and malignant disorders. Single-cell RNA/TCR/BCR profiling with FastMNN integration was performed to define conserved immune cell states. Differential expression, pathway enrichment, and odds-ratio analyses were applied to identify shared transcriptional signatures, while correlation and clustering linked immune programs with clinical indices and drug-target genes. In parallel, flow cytometry was conducted to validate the abundance and phenotype of key immune subsets, and biochip-based protein profiling was used to quantify cytokine and signaling-protein alterations across patient groups.
CAMR and autoimmune diseases shared expansion of SLC8A1⁺ monocytes, ZEB2hi and ANK3⁺CD4⁺ T cells, and aberrant memory B cells (Aber-MBCs). These subsets co-expressed PPP3CA, indicating activation of the calcineurin pathway, FKBP5, reflecting glucocorticoid resistance, and AP-1 components (FOS, JUN, JUND), consistent with stress-adapted and drug-refractory phenotypes. SLC8A1⁺ monocytes in both CAMR and autoimmune cohorts showed increased expression of autophagy-related genes (VPS13B, ATG7), NLRP3 inflammasome components, and JAK–STAT pathway genes, linking metabolic stress to inflammation. Patient-level integration identified two principal molecular modules, AP-1 and calcineurin/JAK–STAT, whose relative activation stratified both CAMR and autoimmune cohorts into biologically and prognostically distinct groups. Drug-target analysis demonstrated that JAK1 was broadly upregulated across immune cell lineages, whereas higher PPP3CA expression together with reduced FKBP1A expression predicted resistance to calcineurin inhibitors, and increased FKBP5 expression indicated reduced glucocorticoid responsiveness, providing a rational framework for mechanism-based therapeutic strategies.
Our cross-disease single-cell framework uncovers convergent immune endotypes linking renal-allograft rejection and systemic autoimmunity. Shared stress-adaptive, NFAT/AP-1–driven, and glucocorticoid-resistant programs explain chronicity and therapeutic refractoriness in both conditions. Integrating these molecular signatures enables precision patient stratification and supports cross-disease drug repurposing, such as using JAK inhibitors for CAMR cases with high JAK1 expression or tacrolimus for autoimmune subtypes characterized by high PPP3CA and FKBP1A expression, thereby advancing personalized management of immune-mediated renal injury.
