Although the precise aetiology of inflammatory bowel disease (IBD) remains unclear, recent discoveries have led to an improved understanding of disease pathogenesis. Whilst these findings have underscored the central role of innate and adaptive immune responses in intestinal inflammation, they have also precipitated a paradigm shift in the key cytokine pathways that drive disease. The prevailing dogma that IBD was mediated by interleukin (IL)-12-driven T-helper (Th)1 CD4 T cell responses towards the bacterial flora has been largely dispelled by findings that the closely related cytokine IL-23 appears to be the key mediator of intestinal inflammation. IL-23 is associated with a novel subset of IL-17-secreting CD4 T cells termed Th17 cells and rodent studies have implicated the IL-23/IL-17 axis in autoimmune inflammation. Genome-wide association studies in IBD patients have confirmed the predominant role of the IL-23 pathway, indicating that this could represent an important future therapeutic target.

中文翻译：

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肠道炎症中的 Interleukin-23 / Interleukin-17 轴。

尽管炎症性肠病 (IBD) 的确切病因尚不清楚，但最近的发现提高了对疾病发病机制的了解。虽然这些发现强调了先天性和适应性免疫反应在肠道炎症中的核心作用，但它们也促成了驱动疾病的关键细胞因子途径的范式转变。IBD 是由白细胞介素 (IL)-12 驱动的 T 辅助 (Th)1 CD4 T 细胞对细菌菌群的反应介导的普遍教条已被发现，即密切相关的细胞因子 IL-23 似乎是关键肠道炎症的介质。IL-23 与一种新的分泌 IL-17 的 CD4 T 细胞亚群相关，称为 Th17 细胞，啮齿动物研究表明 IL-23/IL-17 轴与自身免疫性炎症有关。