Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.
Plasma Cytokine Profles in Ankylosing Spondylitis.
Harper4, Brock E., Weisman1, Michael H., Gourh5, Pravitt, Assassi4, Shervin, Diekman4, Laura A., Ward2, Michael M., Reveille3, John D.
Cedars-Sinai Medical Center, Los Angeles, CA
NIH, NIAMS, IRP, Bethesda, MD
Univ Texas Health Sci Ctr, Houston, TX
Univ. of Texas Health Science Center Houston, Houston, TX
Univ. of Texas Health Science Center Houston
Ankylosing spondylitis (AS) is commonly treated with TNFa inhibitors (TNFi) with success; however, our understanding of the immunology of AS is limited. Identification of the genetic association of IL23R with AS susceptibility implicates involvement of the Th17 pathway in the pathogenesis of AS. This study aims to investigate the possible effects of TNFi use and patterns of lymphocyte activation in AS.
Plasma from 128 AS patients and 144 nonautoimmune controls were obtained from patients seen at the University of Texas Health Science Center at Houston Rheumatology Division within the PSOAS cohort. Levels of 13 cytokines were evaluated by electrochemiluminescent multiplex assays.
AS patients had higher levels of IL-23 (p=0.004), IL-4 (p=0.0007), IL-6 (p<0.0001) and lower levels of IL-1b (p=0.002) and IL-8 (p<0.0001) compared to controls after adjustment for age and gender. Results of analysis of TNFi subsets are shown in Table 1. No differences were seen between either subset of AS patients and controls for IFNg, IL-5, IL-12, IL-13 or IL-10.
Table 1. Comparison of Cytokine Levels in Patients On and Off TNF inhibitors. Cytokine values are listed as mean±SD in pg/mL. P-values are of data after log-transformation and adjustment for age and gender.
|Control (N=144)||AS Off TNFi (N=92)||AS On TNFi (N=36)||Adjusted P value Ctl vs Off||Adjusted P value Ctl vs On||Adjusted P value On vs Off|
|IL 17||1.85 ± 2.27||2.28 ± 2.66||0.61 ± 0||NS||<0.0001||<0.0001|
|IL 23||4.67 ± 12.38||7.65 ± 20.4||10.86 ± 36.97||0.003||NS||NS|
|IL 2||1.80 ± 6.98||1.40 ± 2.88||0.74 ± 0.56||NS||NS||0.008|
|IL 4||1.69 ± 3.08||3.30 ± 4.21||2.40 ± 3.47||<0.0001||0.08||0.05|
|IL 1b||4.93 ± 11.97||1.05 ± 1.98||1.05 ± 1.59||0.006||0.08||NS|
|IL 6||6.19 ± 11.79||15.06 ± 22.27||4.27 ± 7.38||<0.0001||NS||<0.0001|
|IL 8||76.99 ± 343.32||2.82 ± 8.10||4.19 ± 12.00||<0.0001||0.02||NS|
|TNFa||9.73 ± 7.00||11.45 ± 22.48||31.54 ± 31.66||0.0006||<0.0001||<0.0001|
Significant correlations with clinical parameters were found with IL-6 and higher BASDAI, ESR, CRP and limited spinal movement. IL-2 and IL-4 were also associatied with higher BASDAI. IL-17, IL-23, IL-2, IL-4, IL-1b, IL-8 were associated with ESR and CRP.
Plasma cytokines differences between controls and patients with AS particularly with respect to TNFi use support the potential role of dysregulation of the Th17 pathway in AS.
To cite this abstract, please use the following information:
Harper, Brock E., Weisman, Michael H., Gourh, Pravitt, Assassi, Shervin, Diekman, Laura A., Ward, Michael M., et al; Plasma Cytokine Profles in Ankylosing Spondylitis. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1982