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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.
Chronic antibody-mediated kidney rejection (CABMR) is a major cause of chronic allograft injury. Fibroblasts have been implicated in mediating this injury through activation of the interleukin-6 (IL-6) amplifier loop (IL-6 + IL-17), driven by the NFκB and STAT3 signalling pathways. This study investigated the activation of the IL-6 amplifier loop in fibroblasts isolated from renal biopsies of patients with CABMR and evaluated the effects of IL-6 and IL-17 inhibition.
Primary Fibroblasts were cultured from six CABMR patient biopsy samples, purity of the fibroblasts was evaluated using flow cytometry, the fibroblasts were treated with anti-IL-6 (100 ng/mL) and anti-IL-17 (0.75 µg/mL), both before and after stimulation with IL6/sIL-6R (20 ng/µL), IL-17 (50 ng/µL), or combination. ELISA was used to measure IL-6, CCL2, and CCL20 levels in the culture supernatants. The mRNA expression of IL-6, CCL2, CCL20, and SOCS3 was assessed using qPCR, and protein expressions was evaluated by western blot for phosphorylated STAT3 and NFκB p65. Additionally, Serum profiling of 79 kidney transplant recipients and 16 stable graft patients was carried out to evaluate circulating cytokine and chemokine levels associated with allograft rejection, providing insights into immune-mediated mechanisms underlying graft dysfunction.
Synergistic activation of IL-6/sIL-6R and IL-17 signalling markedly amplified fibroblast inflammatory responses, as evidenced by elevated production of IL-6, CCL20, and MCP-1 (p<0.001), along with suppression of the negative regulator SOCS3. This was accompanied by enhanced phosphorylation of NF-κB and STAT3, indicating activation of key pro-inflammatory transcriptional pathways. The combined effect of these cytokines established a self-reinforcing inflammatory circuit that sustains fibroblast activation and cytokine release. Notably, dual inhibition of IL-6 and IL-17 effectively disrupted this amplifier loop, significantly reducing IL-6, CCL20, and MCP-1 secretion, restoring SOCS3 expression, and attenuating NF-κB and STAT3 phosphorylation. Serum profiling revealed elevated IL-6, IL-17, CCL2, and CCL20 levels in the CABMR group compared to SGF, acute TCMR, and ABMR groups. No significant difference was found between acute TCMR and ABMR. Compared to SGF, the acute ABMR group showed higher IL-6, IL-17, and CCL2 levels.
These findings highlight the role of the IL-6 amplifier loop as a potential therapeutic target in CABMR.
