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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.
Tryptophan (TRP) metabolism via the kynurenine pathway produces bioactive metabolites with diverse immunomodulatory effects. While previous studies suggested a role for TRP metabolism in glomerulonephritis (GN), its impact on neutrophil-mediated innate immunity remains poorly understood. We aimed to dissect the distinct contributions of key TRP-metabolizing enzymes and downstream metabolites, focusing on neutrophil function in antibody-mediated GN.
Nephrotoxic serum–induced GN (NTS-GN) was established in C57BL/6 mice deficient in Ido1, Ido2, Kmo, or Kat2. Renal function, histopathology, and TRP metabolites were measured. Neutrophil activation was assessed in vitro using immune complex-coated plates, evaluating morphological spreading, FcγR–dependent Syk phosphorylation, and cytokine secretion. Kynurenic acid (KYNA) was administered intraperitoneally to Ido1-deficient mice and applied to neutrophils in vitro.
Ido1-deficient mice exhibited aggravated renal injury and glomerular neutrophil infiltration, whereas Ido2 deficiency had no effect. Kmo deficiency reduced crescent formation. Unexpectedly, KYNA levels were elevated in the kidneys of Ido1-deficient mice. In these mice, exogenous KYNA administration improved survival, ameliorated renal injury, and reduced neutrophil infiltration. In vitro, KYNA suppressed immune complex–induced neutrophil spreading, attenuated FcγR–Syk phosphorylation, and decreased VEGF secretion in neutrophils derived from Ido1-deficient mice. Additionally, Kat2 deficiency, which abolishes KYNA synthesis, aggravated proteinuria, underscoring KYNA’s protective role.
This study demonstrates that KYNA is a critical modulator of neutrophil-driven inflammation in antibody-mediated GN. By integrating newly established neutrophil in vitro assays and Kat2 knockout analyses, we highlight the TRP–KYNA axis as a promising immunometabolic target for controlling innate immune responses in GN.
