ReviewFrontiers in immunology2026
Exploring the intricate relationship between IL-1β and IL-18 in the context of osteoarthritis.
Review in Frontiers in immunology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 authors.
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Abstract
Interleukin-1β (IL-1β) and interleukin-18 (IL-18) are key members of the IL-1 cytokine family that contribute to the initiation and progression of osteoarthritis (OA). Although both cytokines share structural similarities and use MyD88-dependent signaling pathways, accumulating evidence indicates that they function complementarily rather than redundantly. IL-1β acts as an early catalyst for catabolic processes, leading to cartilage breakdown and cellular senescence, whereas IL-18 serves as an inflammasome-dependent enhancer that activates the immune response. This review summarizes the roles of IL-1β and IL-18 at multiple biological levels in OA progression and discusses their secretion and activation mechanisms. Additionally, we explore current and emerging pathological strategies that target the effects of IL-1β and IL-18 on resident cells during knee OA progression. Despite substantial evidence suggesting that cytokines are involved in OA progression, IL-1β-targeted therapies have shown limited clinical success, highlighting the need to explore additional targets. By integrating multiple pathological mechanisms, this review proposes a conceptual framework in which OA progression comprises three interconnected phases: cytokine-driven initiation, amplification, and chronicity, all linked to senescence. In conclusion, this review evaluates current pharmacological strategies. It underscores future research directions that focus on key elements of the IL-1β/IL-18 signaling pathway, emphasizing the significance of biomarker-driven and combination therapies for improving OA management.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.