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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.
Despite advances in lupus nephritis (LN) management, many patients fail to respond to first-line therapy or relapse after remission. Overexpression of P-glycoprotein (p-gp) on Plasma cells (PCs) and T-helper 17 lymphocytes (Th17) cells may contribute to disease activity and a drug-resistant phenotype in lupus nephritis (LN). P-gp has been linked to corticosteroid resistance. Emerging evidence suggests IL-17 signaling through the TAK-1/C/EBP-β axis may modulate P-gp expression.
Objective: Evaluation of role of downstream IL-17 mediated pathway (IL-17/TAK-1/C/EBP-β pathway) in upregulation of P-gp expression in PCs and lymphocytes of LN and their contribution in the refractoriness to immunosuppressive treatment.
We analyzed peripheral blood PCs and Th17 cells for P-gp expression in LN patients. U266B1 plasma cells were treated with IL-17, IL-6, and their inhibitors—anti-IL-6 + anti-IL-17, IL-17 + (5Z)-7-oxozeaenol (TAK-1 inhibitor), and IL-17 + ST101 (C/EBP-β inhibitor)—for 24 hours. Plasma levels of NGAL, IL-17, IL-6, TNF-α, CXCL12, and CXCL13 were quantified by ELISA.
49 LN patients (refractory n=11; active n=20; inactive n=18) and 15 healthy controls were studied. Frequencies of CD38⁺CD138⁺ PCs, and P-gp⁺ PCs, Th17, P-gp⁺Th17, were significantly elevated in refractory and active LN compared with inactive LN and controls, which decreased after 3 months of standard therapy. IL-17, IL-6, TNF-α, CXCL12, and NGAL levels were elevated in plasma and declined post-treatment (P<0.001). In vitro, IL-6 + IL-17 stimulation induced P-gp expression in plasma cell line , In pre treatment stretegy, expression of P-gp was significantly suppressed by anti-IL-6 + anti-IL-17, or by IL-17 inhibition combined with (5Z)-7-oxozeaenol or ST101.While, in the post treatment streategy, expression of P-gp was not significantly decreased when treated with anti-IL-6 + anti-IL-17 or IL-17 inhibition combined with (5Z)-7-oxozeaenol or ST101.
In refractory LN, elevated P-gp–expressing PCs and Th17⁺P-gp lymphocytes contribute to treatment resistance. IL-17 induces P-gp via the TAK-1 pathway, while inhibition of IL-17 signaling reduces P-gp expression. Thus, targeting the downstream IL-17mediated pathway in PCs may offer a therapeutic strategy for refractory LN.
