The Journal of Practical Medicine ›› 2025, Vol. 41 ›› Issue (18): 2953-2960.doi: 10.3969/j.issn.1006-5725.2025.18.024

• Reviews • Previous Articles    

Research progress on Th17 cell differentiation regulation mechanisms and therapeutic targets in ankylosing spondylitis

Mingyang YU,Jia LI,Xinzhe FENG,Jingjing BI,Cheng LI()   

  1. Department of Joint Orthopedics,the First Affiliated to the Naval Military Medical University,Shanghai 200433,Shanghai,China
  • Received:2025-07-01 Online:2025-09-20 Published:2025-09-25
  • Contact: Cheng LI E-mail:drlicheng@sina.com

Abstract:

Ankylosing spondylitis (AS) is a chronic autoimmune disease characterized by inflammatory involvement of the axial skeleton and pathological bone formation. The T helper 17 cell (Th17 cell) subset of lymphocytes plays a central role in mediating the inflammatory processes associated with AS. This review summarizes recent advances in the regulation of Th17 cell differentiation in AS, with a focus on the complex mechanisms governed by cytokine microenvironments, transcription factor networks, and metabolic and epigenetic regulatory pathways. Key regulatory components discussed include the IL-23/STAT3 signaling axis, the CCL20/CCR6 chemotactic axis, and the master transcription factor RORγt. Additionally, this review critically evaluates emerging therapeutic strategies targeting metabolic reprogramming (e.g., PKM2), epigenetic regulators (e.g., JMJD3, EZH2), engineered exosome delivery systems, and modulators of metabolic enzymes. By analyzing the limitations of current treatment approaches, the review proposes future research directions emphasizing multi-target therapeutic strategies and highlights the importance of personalized medicine in achieving precise and effective treatment for AS. These developments reveal promising new avenues for modulating Th17-mediated immunity, offering transformative potential for the clinical management of AS.

Key words: ankylosing spondylitis, Th17 cells, IL-23/IL-17 axis, signaling pathways, targeted therapy, transcriptional regulation, bone remodeling

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