IL-23 is a key cytokine in the pathogenesis of spondyloarthritides, including PsA and axial spondyloarthritis, as well as related conditions, such as psoriasis and IBD. Genetic associations, animal models and translational studies in humans demonstrate the key role played by IL-23, especially when coupled with downstream overexpression of IL-17 via stimulation of T helper 17 (Th17) and other cells by IL-23. Whereas IL-23 inhibition has shown clear-cut benefit in psoriasis and peripheral manifestations of PsA, trials of IL-23 inhibitors have failed in the treatment of ankylosing spondylitis. More recently, exploratory data from PsA patients with axial symptoms suggests that improvement may occur, but needs confirmation in dedicated axial spondyloarthritis (axSpA) trials. Hypotheses for these apparently conflicting findings about IL-23 inhibition in various forms of spondylitis are discussed.

中文翻译：

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IL-23 和轴性疾病：它们会同时发生吗？


IL-23 是脊柱关节炎（包括 PsA 和中轴型脊柱关节炎）以及相关病症（例如牛皮癣和 IBD）发病机制中的关键细胞因子。遗传关联、动物模型和人类转化研究证明了 IL-23 发挥的关键作用，特别是当 IL-23 通过刺激 T 辅助细胞 17 (Th17) 和其他细胞与下游 IL-17 过度表达结合时。虽然 IL-23 抑制已在银屑病和 PsA 外周表现中显示出明显的益处，但 IL-23 抑制剂在治疗强直性脊柱炎方面的试验却失败了。最近，来自患有中轴症状的 PsA 患者的探索性数据表明，可能会出现改善，但需要专门的中轴型脊柱关节炎 (axSpA) 试验来证实。讨论了关于各种形式的脊柱炎中 IL-23 抑制的这些明显相互矛盾的发现的假设。