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The relation of cytokines of IL-17/IL-23 axis to Th1/Th2 cytokines and disease activity in systemic lupus erythematosus

Abstract

INTRODUCTION: Interleukin (IL)-17 is recently linked to the pathogenesis of systemic lupus erythematosus (SLE) but its relation to disease activity has not been well characterised. The objectives of this study were to examine the relation of serum cytokine levels from the IL-17/IL-23 axis (IL-17, IL-23) to Th1 (IL-12, IFN-γ), Th2 (IL-10, IL-6, IL-4) cytokines and disease activity in SLE patients. METHODS: Serum cytokines were measured by enzyme-linked immunosorbent assays. Disease activity was determined by SLE disease activity index (SLEDAI), anti-dsDNA antibody, C3 and C4 levels. RESULTS: Serum levels of IL-17, IL-10 and IFN-γ were higher in SLE patients (n=70) compared to age- and sexmatched controls (n=14) [P<0.001]. Higher serum IL-23 level was found in active lupus patients who had cutaneous manifestation (P=0.003) and serositis (P=0.03) compared to those who had not. Serum IL-17 was not different between patients who had active lupus nephritis (n=23), non-renal active lupus (n=13) and inactive disease (n=34) [P=0.23]. However, an inverse correlation between serum IL-17 with proteinuria was found among all SLE patients (r= –0.27, P=0.03). Serum IL-17 level was, otherwise, not related to SLEDAI, glomerular filtration rate, activity or chronicity score and ISN/RPS class among patients with active lupus nephritis and was not found to correlate with serum IFN-γ or IL-10. CONCLUSIONS: Elevated serum IL-23 was found in patients with inflammatory manifestations including cutaneous involvement and serositis. Serum IL-17 level was not shown to correlate with disease activity but demonstrated an inverse correlation with proteinuria suggesting urinary loss of IL-17 and its involvement in lupus renal pathology.published_or_final_versionThe 15th Medical Research Conference (15th MRC), Department of Medicine, University of Hong Kong, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16 n. 1, suppl. 1, p. 45, abstract no. 7

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