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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.
Lupus nephritis (LN), a severe manifestation of systemic lupus erythematosus, involves persistent immune complex deposition and complement overactivation. Mannose binding lectin associated serine protease 2 (MASP-2) and MASP-3 regulate the lectin and alternative complement pathways, respectively. MASP-2 cleaves complement components C4 and C2 to initiate the lectin pathway, while MASP-3 activates pro–Factor D to propagate alternative pathway amplification. Although MASP proteins are implicated in lupus pathogenesis, their specific and combined roles in established LN remain undefined. This study aimed to evaluate the therapeutic effects of MASP-2, MASP-3, and dual MASP-2/3 inhibition in a pristane induced murine model of LN.
Female BALB/c mice were induced with lupus via intraperitoneal pristane injection and monitored for 6 months until serologic and renal disease features emerged. Mice were then randomized (n=8 per group) to receive intravenous MASP-2 monoclonal antibody, MASP-3 monoclonal antibody, a combined MASP-2/3 polyclonal preparation (5 mg/kg total), or saline as vehicle control, administered twice per week for 4 weeks. Serum anti–double stranded DNA (anti-dsDNA) antibodies, complement C3, blood urea nitrogen (BUN), creatinine, and urine albumin to creatinine ratio were assessed weekly. At sacrifice, kidneys were evaluated for histology, immune cell infiltration, complement deposition, and transcriptomic changes using bulk RNA sequencing with gene set enrichment analysis.
Dual MASP-2/3 blockade significantly reduced anti-dsDNA antibody levels at week 2 and lowered BUN by weeks 2–3 compared to vehicle. Albuminuria was decreased in MASP-3 and MASP-2/3 groups from week 2 onward. C3 levels were preserved in all treatment groups, with MASP-2/3 showing the greatest effect. Creatinine showed a downward trend but without statistical significance. Lectin pathway activity was reduced in the MASP-2 and MASP-2/3 groups, while alternative pathway activity was not significantly altered. Immunohistochemistry revealed reduced renal CD4⁺ T cell and CD68⁺ macrophage infiltration in the MASP-2/3 group. Complement deposition of C4d, C3c, membrane attack complex (MAC, C5b-9), and Factor D was markedly attenuated in the MASP-2/3 group. Transcriptomic analysis of kidney tissue showed suppression of inflammatory gene expression and significant enrichment of the peroxisome proliferator activated receptor (PPAR) signaling pathway in the MASP-2/3 group, suggesting a shift toward anti-inflammatory and metabolic reprogramming.
Combined MASP-2 and MASP-3 inhibition offers superior therapeutic benefit in established lupus nephritis compared to single agent strategies. Dual blockade not only reduces serologic disease activity and complement deposition but also preserves complement homeostasis and attenuates renal immune cell infiltration. Notably, transcriptional analysis revealed downregulation of the PPAR signaling pathway, implicating a mechanistic link between complement regulation and metabolic modulation in the inflamed kidney. These findings support MASP proteins as promising therapeutic targets and support further investigation of dual MASP-2/3 inhibition in clinical lupus nephritis.
