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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.
The specific pathogenesis of renal light chain amyloidosis (AL) has not yet been elucidated. This study was designed to analyze plasma cell characteristics of renal AL by single cell sequencing, and explored the potential critical signaling pathways and molecules in renal AL.
Five patients with renal AL were selected and their bone marrow mononuclear cells (BMMCs) and peripheral blood mononuclear cells (PBMCs) were collected, and three healthy individuals were used as control. Plasma cell sorting was performed in the samples of patients. Combined with single-cell RNA-seq and scVDJ-seq techniques, the critical molecules in specific signal passway were explored and verified in vivo and in vitro.
Single-cell sequencing analysis showed that BMMCs from patients with renal AL showed unique transcriptome characteristics compared with healthy controls. Most up-regulated genes are involved in encoding immunoglobulins (IGLV, IGKV, IGHV, JCHAIN), regulation of plasma cell differentiation, antibody synthesis and secretion (MZB1, XBP1), proper folding, degradation and transport of endoplasmic reticulum proteins (HSP90B1, HSPA5, SSR4, DERL3, SDF2L1), and endoplasmic reticulum isomerase activity (TXNDC5, FKBP11, FKBP2) pathways, with marginal zone B and B1 cell-specific protein (MZB1) being significantly up-regulated in BMMCs and PBMCs of AL patients. Further analysis revealed that there were clonally expanded subpopulations of BMMCs of AL patients, whose gene expression profiles showed individual heterogeneity, and gene expression differences existed between plasma cell subpopulations secreting kappa light chain (LC) and lambda LC. Interestingly, only MZB1 was found co-localized with mesangial cells as well as BMMCs a in patients of type lambda AL. Importantly, MZB1 was found significantly down-regulated in BMMCs after treatment compared to that of before treatment. In vivo, MZB1 was found markedly up-regulated in mesangial cells of patients of AL-lambda compared to controls. In vitro, MZB1was revealed significantly up-regulated in rat mesangial cells (HBZY-1 cells) stimulated by purified human lambda LC protein. In contrast, knockdown MZB1 alleviated the lambda LC-induced HBZY-1 cells apoptosis by inhibition of caspase 7.
Current study provides new ideas for in-depth exploration of the pathogenesis of renal AL that MZB1/casapase7 inhibits LC induced apoptosis of mesangial cells, consequently, contributes to the development of renal AL.
