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Rheumatology Advance Access published online on May 28, 2009
Rheumatology, doi:10.1093/rheumatology/kep125
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Differential cytokine profiles in juvenile idiopathic arthritis subtypes revealed by cluster analysis

Henk-Jan van den Ham1, Wilco de Jager2, Johannes W. J. Bijlsma3, Berent J. Prakken2 and Rob J. de Boer1

1Theoretical Biology and Bioinformatics, Utrecht University,2Department of Paediatric Immunology and 3Department of Rheumatology and Clinical Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands

Correspondence to: Henk-Jan van den Ham, Theoretical Biology and Bioinformatics, Utrecht University, Padualaan 8, 3584 CH, Utrecht, The Netherlands. E-mail: h.j.vandenham{at}uu.nl


  Abstract

Objectives. With the introduction of high-throughput biomarker measurements, traditional analysis of these markers is increasingly difficult. Using samples from a diverse group of patients, we tested the applicability of cluster analysis to these data. Using this method, we aim to visualize some of the patterns specific to certain disease groups. In particular, we focus on juvenile idiopathic arthritis (JIA), a multifactorial autoimmune disorder that ultimately leads to chronic inflammation of the joints.

Methods. Cytokine measurements were performed using multiplex immunoassays. Using heuristic clustering methods, we set out to compare the pattern of 30 cytokines in plasma and SF of JIA, RA, OA, or diabetes type II patients and healthy controls.

Results. Analysis shows that oligo- and polyarticular JIA have similar biomarker profiles, both in plasma and SF. Systemic onset JIA (SoJIA) has a profile distinct from other JIA subtypes, suggesting that they involve different inflammatory processes. SoJIA samples do, however, cluster together with RA in SF, suggesting that these two conditions have similar cytokine profiles. Furthermore, we identify several clusters of ILs and chemokines that are co-expressed, suggesting that they are co-regulated.

Conclusions. We show that previously undetected clusters of cytokines and patients can be identified by applying cluster analysis to multiplex data. Cytokine clusters identified in plasma and SF samples were quite different, which underscore the differential cytokine signalling in these two compartments, and suggest that plasma samples may not be suitable for estimating joint biomarker profiles and inflammation.

KEY WORDS: Juvenile idiopathic arthritis, Cluster analysis, Inflammation, Cytokines, Biomarkers

Submitted 6 October 2008; Accepted 20 April 2009


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