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[Spondyloarthritis].

U Syrbe1,2, X Baraliakos3

  • 1Medizinische Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200, Berlin, Deutschland. uta.syrbe@charite.de.

Zeitschrift Fur Rheumatologie
|May 17, 2018
PubMed
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See all related articles

Spondyloarthritis (SpA) involves joint inflammation, influenced by genetics like HLA-B27 and the IL-23/IL-17 pathway. Gut inflammation and microbiota also play a role in SpA development and progression.

Area of Science:

  • Rheumatology
  • Immunology
  • Genetics

Background:

  • Spondyloarthritis (SpA) is a group of inflammatory diseases affecting axial and peripheral joints, enthesitis, and dactylitis.
  • Genetic factors, particularly HLA-B27, strongly influence SpA development, with transgenic models showing a direct role.
  • The interleukin (IL)-23/IL-17 signaling pathway is implicated, supported by the efficacy of IL-17 inhibitors.

Purpose of the Study:

  • To summarize the key genetic and immunological factors contributing to Spondyloarthritis (SpA).
  • To highlight the role of the gut microbiome and inflammation in SpA pathogenesis.
  • To discuss the histopathological findings in axial SpA and ongoing research into disease mechanisms.

Main Methods:

  • Review of genetic associations, including HLA-B27 and genome-wide association studies.
Keywords:
Ankylosing spondylitisHLA-B27Interleukin-17Interleukin-23Signal pathways

Related Experiment Videos

  • Analysis of the interleukin (IL)-23/IL-17 signaling pathway's role.
  • Examination of histopathological findings in axial SpA and the impact of gut inflammation.

    • Main Results:

    • HLA-B27 is a major genetic determinant for SpA.
    • Polymorphisms in immune function genes, especially in the IL-23/IL-17 pathway, are associated with SpA.
    • Gut inflammation and commensal microbiota appear to contribute pathogenically to SpA.

    Conclusions:

    • SpA pathogenesis is multifactorial, involving genetic predisposition (HLA-B27), immune pathways (IL-23/IL-17), and gut microbiome interactions.
    • Understanding these mechanisms is crucial for developing targeted therapies.
    • Further research is needed to elucidate how genetic and gut factors interact at sites of mechanical stress.