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301 Evidence for a pro-inflammatory as well as protective role for il-17a in patients with systemic lupus erythematosus
  1. W Raymond1,
  2. G Ostli-Eilertsen2,
  3. S Griffiths1 and
  4. J Nossent1,2
  1. 1The University of Western Australia, School of Medicine- Rheumatology section, Perth, Australia
  2. 2Arctic University Norway, Dept Internal Medicine – Bone and Joint group, Tromso, Norway

Abstract

Background and aims The successful application of IL-17 inhibitors in a number of chronic inflammatory diseases has increased interest for the role of IL-17 in other conditions. We investigated the clinical associations for the predominant family member IL-17A in patients with Systemic Lupus Erythematosus (SLE).

Methods Cross-sectional study of SLE patients (n=102, age 49, 86% female) recruited from a regional registry. IL-17A levels were determined by immunoassay, disease activity by SLEDAI-2K and cumulative damage by SLICC-DI scores. Non-parametric techniques were used to examine the association between IL-17A and disease activity, autoantibody profiles and damage development in SLE patients and for comparisons with healthy controls (n=31).

Results SLE patients had higher IgG levels, lower T cell and B cell counts, but median IL-17A levels did not differ from controls (28.4 vs. 28.4 pg/ml, p=0.9).

In SLE patients, IL-17A levels did not correlate with SLEDAI-2K or SDI, but were inversely related with systolic blood pressure (r=−0.31, p=0.02), years smoking (r=−0.23, p<0.001), cumulative heart (r=−0.24, p=0.03) and malignancy damage (r=−0.18, p=0.06).

Serological correlations for IL-17A existed with levels of IgG (r=0.21, p=0.05), hs-CRP levels (r=0.28, p<0.01), proteinuria (r=0.64, p=0.004) and pre-albumen (r=−0.22, p=0.03).

Longitudinal data showed only modest fluctuations in 17A levels, unrelated to SLEDAI-2K

Conclusions These data indicate that while IL-17A participates in the inflammatory process in SLE, it also seems to serve a protective purpose in reducing heart disease and cancer in SLE. This dual role is consistent with experimental and clinical data and raises concerns about inhibting IL-17 in SLE patients.

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