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Extended report
From gene expression to serum proteins: biomarker discovery in ankylosing spondylitis
  1. N Haroon1,2,
  2. F W L Tsui1,2,
  3. F D O’Shea1,2,
  4. B Chiu1,
  5. H W Tsui1,
  6. H Zhang3,
  7. K W Marshall1,2,3,
  8. R D Inman1,2
  1. 1
    Toronto Western Research Institute, Ontario, Canada
  2. 2
    University of Toronto, Toronto, Ontario, Canada
  3. 3
    GeneNews Limited, Richmond Hill, Ontario, Canada
  1. Correspondence to Dr R D Inman, Arthritis Center of Excellence, Toronto Western Hospital, 399 Bathurst St, Toronto, ON M5T 2S8, Canada; robert.inman{at}


Objectives: Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).

Methods: Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)–PCR. Corresponding serum-soluble LIGHT (sLIGHT) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index.

Results: Post-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRT–PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R  =  0.60; p = 0.01) and ESR (R  =  0.51; p = 0.04). The fold change in sLIGHT correlated with change in both CRP (R  =  0.71, p = 0.002) and ESR (R  =  0.77, p<0.001).

Conclusion: LIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers.

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  • Competing interests None.

  • Ethics approval The study was approved by the University Health Network ethics board.

  • Patient consent Obtained.