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Spondyloarthritis in 2012: Advances in pathogenesis through animal models and imaging

Walter P Maksymowych1

  • 1Division of Rheumatology, Department of Medicine, 562 HMRB, University of Alberta, Edmonton, Alberta T6G 2S2, Canada. walter.maksymowych@ualberta.ca.

Nature Reviews. Rheumatology
|January 9, 2013
PubMed

Insights

Recent advances clarify spondyloarthritis mysteries, explaining T-cell therapy limits and the IL-23-IL-17 axis role in disease pathology. Anti-TNF treatments may offer a brief window to impact inflammatory lesions.

Area of Science:

  • Immunology
  • Rheumatology
  • Molecular Biology

Background:

  • Spondyloarthritis (SpA) pathogenesis remains incompletely understood.
  • The efficacy of T-cell-directed therapies has been suboptimal.
  • The role of the interleukin-23 (IL-23) to interleukin-17 (IL-17) cytokine axis in SpA is a key area of investigation.

Purpose of the Study:

  • To elucidate the reasons behind the limited efficacy of T-cell-directed therapies in SpA.
  • To clarify the specific involvement of the IL-23-IL-17 cytokine axis in SpA pathology.
  • To assess the therapeutic window for anti-tumor necrosis factor (anti-TNF) agents in managing SpA inflammatory lesions.

Main Methods:

  • Review of recent advancements in SpA research up to 2012.
  • Analysis of immunological pathways involved in SpA.
  • Evaluation of therapeutic strategies including T-cell-directed therapies and anti-TNF agents.

Main Results:

  • Advances have resolved key questions regarding T-cell therapy limitations in SpA.
  • The critical link between the IL-23-IL-17 cytokine axis and SpA pathology has been established.
  • The window of opportunity for anti-TNF agents to influence disease progression at inflammatory sites appears transient.

Conclusions:

  • Understanding the IL-23-IL-17 axis is crucial for SpA treatment.
  • Future SpA therapies may need to target this cytokine pathway more effectively.
  • The timing of intervention with anti-TNF agents is critical for managing SpA.

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