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Related Experiment Video

Updated: Jun 5, 2025

Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice
04:47

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Ankylosing spondylitis: From pathogenesis to therapy.

Yuxiao Wei1, Shuqiong Zhang1, Fenli Shao2

  • 1State Key Laboratory of Pharmaceutical Biotechnology, Chemistry and Biomedicine Innovation Center (ChemBIC), School of Life Sciences, Nanjing University, 163 Xianlin Avenue, Nanjing 210023, Jiangsu, China.

International Immunopharmacology
|December 7, 2024
PubMed
Summary
This summary is machine-generated.

Ankylosing spondylitis (AS) pathogenesis involves genetic factors, gut microbiota autoantigens, and bone metabolism. Understanding these complexities aids in identifying novel therapeutic targets for this autoimmune rheumatic disease.

Keywords:
Ankylosing spondylitisPathogenesisTherapeutic targetsTreatment

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Area of Science:

  • Rheumatology
  • Immunology
  • Genetics

Background:

  • Ankylosing spondylitis (AS) is an autoimmune rheumatic disease affecting axial joints with complex, incompletely understood etiology.
  • Current treatments focus on inflammation management, yielding inconsistent results due to patient heterogeneity.

Purpose of the Study:

  • To systematically review the pathogenesis of AS, including genetic susceptibility, autoimmune responses, and bone metabolism.
  • To discuss current management strategies, risk factors, and potential therapeutic targets for AS.

Main Methods:

  • Systematic literature review of pathogenesis and management of Ankylosing Spondylitis.
  • Analysis of genetic factors (HLA-B27), immune signals (Th17), autoantigens (gut microbiota), and bone metabolism.

Main Results:

  • AS etiology involves HLA-B27, Th17 signals, gut-derived autoantigens, T-cell receptor interactions, and dysregulated bone metabolism.
  • Pathological new bone formation is promoted by altered bone metabolism in AS patients.
  • Current treatments targeting inflammation show variable efficacy.

Conclusions:

  • Further research into AS pathogenesis, including autoantigen-centered responses and bone stromal cell influence, is crucial.
  • Identifying novel therapeutic targets beyond inflammation management is needed to address AS heterogeneity and improve treatment outcomes.