ISSN 2147-9720 | E-ISSN 2148-4279
Original Article
IL-17A levels in systemic lupus erythematosus associated with inflammatory markers and lower rates of malignancy and heart damage: Evidence for a dual role
1 Rheumatology Group, The University of Western Australia School of Medicine, Crawley, Western Australia  
2 Department of Clinical Medicine, Bone & Joint Group, Arctic University, Tromsø, Norway  
3 Rheumatology Group, The University of Western Australia School of Medicine, Crawley, Western Australia; Department of Clinical Medicine, Bone & Joint Group, Arctic University, Tromsø, Norway  
Eur J Rheumatol 2017; 4: 29-35
DOI: 10.5152/eurjrheum.2017.16059
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Key Words: IL-17A, Systemic Lupus Erythematosus, SLEDAI, organ damage
Abstract

Objective: The interleukin 17 (IL-17) cytokine family is involved in a number of chronic inflammatory diseases. In spite of contradictory findings and a lack of causality in clinical studies, IL-17 inhibition for systemic lupus erythematosus (SLE) has regained attention as a potential therapeutic pathway, after demonstrating disease-modifying capabilities in ankylosing spondylitis. We investigated the clinical associations of interleukin 17 A (IL-17A) in patients with SLE.

 

Material and Methods: A cross-sectional study was performed involving SLE patients (n=102; age: 49 years; 86% female) recruited from a regional registry. IL-17A levels were determined by immunoassay, disease activity by Systemic Lupus Erythematosus Disease Activity Index-2K (SLEDAI-2K), and cumulative damage by Systemic Lupus International Collaborative Clinics Damage Index (SDI) scores. Non-parametric techniques were used to examine the association between IL-17A and disease activity and autoantibody profiles were compared with healthy controls (n=31): principal component analysis (PCA) was used to determine the interplay of immune cells across disease states and damage development in SLE patients.

 

Results: SLE patients had higher IgG levels, lower T-cell and B-cell counts, but median IL-17A levels did not differ from the controls (28.4 vs. 28.4 pg/mL, p=0.9). In SLE patients, IL-17A did not correlate with SLEDAI-2K or SDI, but was inversely related with age (correlation coefficients, Rs.=–0.29, p<0.05), systolic blood pressure (Rs.=–0.31, p<0.05), years of smoking (Rs.=–0.43, p<0.05), cumulative heart (Rs.=–0.22, p<0.05), and malignancy damage (Rs.=–0.18, p<0.05). Serological correlations for IL-17A existed with immunoglobulin G (IgG) levels (Rs.=0.21, p<0.05), high sensitivity C-reactive protein (hs-CRP) levels (Rs.=0.28, p<0.05), proteinuria (Rs.=0.64, p<0.05), and pre-albumin (Rs.=–0.22, p<0.05). Longitudinal data showed only modest fluctuation in IL-17A levels, independent of SLEDAI-2K.

 

Conclusion: These results suggest that IL-17A, while participating in inflammation, may also serve a protective purpose in SLE patients.

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