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.
Lupus nephritis (LN) is a major organ manifestation of systemic lupus erythematosus (SLE), in which immune-complex (IC) deposition and inflammatory cell infiltration contribute to disease progression. We previously showed that IgG from patients with LN directly injures podocytes via a Ca2+/calmodulin-dependent kinase IV (CaMK4) pathway, independent of immune cells. Podocyte uptake of IgG involves the neonatal Fc receptor (FcRn), and FcRn inhibition reduces IgG internalization. While FcRn maintains circulating IgG and is targeted therapeutically in other autoimmune diseases, its role in LN remains unclear. We aim to investigate whether FcRn in glomerular cells initiates IgG-driven podocyte injury and delineated FcRn-dependent mechanisms across glomerular cells, including mesangial cells.
We generated an imiquimod-induced lupus model in systemic FcRn-knockout (KO) and wild-type (WT) mice and compared renal phenotypes. Leukocyte subsets in kidney, spleen, and peripheral blood were analyzed by flow cytometry. We also created podocyte-specific FcRn-KO mice and performed similar evaluations. In vitro, human immortalized podocytes and primary mesangial cells isolated from systemic FcRn-KO and WT mice were stimulated with ICs prepared using sera from patients with LN, sera from lupus-model mice, or 4-hydroxy-3-nitrophenylacetyl-ovalbumin. Readouts included LN-relevant inflammatory mediators (e.g., cytokine production).
In systemic FcRn-KO mice, imiquimod-induced proteinuria was attenuated versus WT, whereas some WT mice developed endocapillary proliferative lesions. Serum IgG and anti-double-stranded DNA antibody levels were significantly lower in FcRn-KO mice. However, glomerular IgG and C3 deposition—predominantly mesangial—did not differ between groups. Spleen weight and leukocyte subset distributions in spleen and peripheral blood were comparable. These findings suggest that FcRn-dependent responses within glomerular resident cells to ICs, rather than systemic immune activation itself, drive proteinuria. In podocyte-specific FcRn-KO mice, proteinuria and histopathology were not different from controls. In vitro, IC stimulation of mesangial cells lacking FcRn resulted in reduced inflammatory cytokine expression compared with WT mesangial cells.
Systemic loss of FcRn mitigates proteinuria in an imiquimod-induced lupus model without altering glomerular IC deposition, implicating FcRn-mediated IC sensing within glomerular resident cells. Our data indicate that mesangial—rather than podocyte—FcRn promotes pro-inflammatory cytokine production and contributes to LN progression. Targeting mesangial FcRn may therefore represent a therapeutic strategy to limit glomerular inflammation and proteinuria in LN.
