棘球蚴病是一种广泛分布的人畜共患疾病，其发病隐匿，潜伏期长，严重威胁人类健康。其免疫逃逸与宿主免疫系统相互作用复杂，特别是辅助性T(Th)细胞亚群及其分泌的细胞因子在疾病进展中起关键作用。本文综述IL-23/IL-17轴在棘球蚴病中的作用。IL-23由活化的树突状细胞和巨噬细胞分泌，可促进Th17细胞分化并分泌IL-17。研究表明，在细粒棘球蚴病中，IL-23和IL-17水平变化与感染阶段和免疫反应密切相关，且受药物干预影响；在多房棘球蚴病中，IL-23和IL-17在感染早期上升，晚期与疾病活动性相关。IL-23/IL-17轴通过JAK/STAT信号通路调节炎症反应和免疫细胞功能，在棘球蚴病的免疫调节中发挥重要作用。进一步研究该轴在棘球蚴病中的作用机制，有助于开发新的治疗靶点和生物标志物，为棘球蚴病的早期诊断、预后评估和免疫治疗提供新思路。

Echinococcosis is a zoonotic parasitic disease that is distributed widely around the world, with hidden onset and long incubation period, which seriously threatens human health. The interaction between immune escape and host immune system is complex, and especially the helper T(Th) cell subsets and their secreted cytokines play a key role in disease progression. In this article, the role of IL-23/IL-17 axis in echinococcosis was reviewed. IL-23 is secreted by activated dendritic cells and macrophages, which can promote the differentiation of Th17 cells and secrete IL-17. Studies have shown that the changes of IL-23 and IL-17 levels in cystic echinococcosis are closely associated with the infection stage and immune response, and affected by drug intervention. In alveolar echinococcosis, IL-23 and IL-17 levels are increased in the early stage of infection, and are associated with disease activity in the late stage. IL-23/IL-17 axis can regulate inflammatory response and immune cell function through the JAK/STAT signaling pathway, which plays an important role in immune regulation of echinococcosis. Further study of the mechanism underlying IL-23/IL-17 axis in echinococcosis will contribute to developing novel therapeutic targets and biomarkers, providing new ideas for early diagnosis, prognostic evaluation and immunotherapy of echinococcosis.