ArticleInflammation2026
IL-18 Promotes the Development of Lupus Nephritis by Activating the Wnt/β-Catenin Signaling Pathway in Renal Tubular Epithelial Cells.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study investigates the specific role of interleukin-18 (IL-18) in lupus nephritis (LN) progression and its molecular mechanisms to provide a theoretical basis for the pathological intervention of LN. IL-18 levels were measured from systemic lupus erythematosus (SLE) patients with or without LN. MRL/lpr mice received intraperitoneal injection of IL-18 or its inhibitor to assess renal injury, inflammation, and Wnt/β-catenin pathway activity. In-vivo intervention experiments using Caspase-1 inhibitor (Ac-YVAD-CMK), Wnt pathway agonists (BML-284), and inhibitors (IWR-1-endo) were performed. In-vitro studies were conducted in human renal tubular epithelial cell line HK-2 to investigate the molecular mechanisms. IL-18 was markedly elevated in SLE patients, and further increased in urine and renal tissue of LN. In MRL/lpr mice, exogenous IL-18 significantly exacerbated renal injury, evidenced by increased urinary protein, serum creatinine, anti-dsDNA antibodies, tubulointerstitial inflammation, and increased activity index. This was accompanied by up-regulation of IFN-γ, IL-1β, IL-6, down-regulation of IL-10, and activation of the Wnt/β-catenin pathway (increased β-catenin, p-GSK-3β, and CK1α). Conversely, IL-18 blockade or Wnt inhibition attenuated these pathological changes. Notably, the protective effects of IL-18 inhibition were reversed by simultaneous Wnt activation. In-vitro, IL-18 promoted HK-2 cell proliferation and inflammatory secretion by activating Wnt/β-catenin signaling, effects which were blocked by a Caspase-1 inhibitor or a Wnt pathway inhibitor. IL-18 activated the Wnt/β-catenin signaling pathway in renal tubular epithelial cells and disrupted the balance of pro- and anti-inflammatory cytokine networks, thereby exacerbating tubulointerstitial inflammation and promoting renal injury in LN mice. These findings highlight the therapeutic potential of targeting the IL-18 signaling pathway in LN. Trial registration: Not applicable.
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