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Chinese Journal of Hepatic Surgery(Electronic Edition) ›› 2026, Vol. 15 ›› Issue (03): 426-432. doi: 10.3877/cma.j.issn.2095-3232.2026.03.019

• Review • Previous Articles    

Research progress in IL-23/IL-17 axis in echinococcosis

Rongdong He1,2, ·Tuxun Tuerhongjiang1,2, Hao Wen1,2,()   

  1. 1 Department of Liver and Laparoscopic Surgery, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China
    2 State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Urumqi 830054, China
  • Received:2025-11-12 Online:2026-06-10 Published:2026-06-05
  • Contact: Hao Wen

Abstract:

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.

Key words: Echinococcosis, IL-23/IL-17 axis, Immunomodulation, T-lymphocytes

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