Abstract

Objectives To analyze the correlation between the serum concentration of interleukin- (IL-) 23 and atherosclerotic changes, traditional atherosclerotic risk factors, the autoantibody profile, and involvement of selected organs in systemic lupus erythematosus (SLE) patients. Patients and Methods We studied 94 SLE patients and 27 controls. We analyzed the IL-23 serum concentration, autoantibodies, carotid intima-media thickness and atherosclerotic plaque, the ankle-brachial index, atherosclerotic risk factors, and organ manifestations. Results Concentrations of IL-23 significantly differed between SLE patients and the controls (p = 0.0015). On the basis of multivariate stepwise analysis, we revealed that high levels of IL-23 were associated with atherosclerotic plaque in common femoral arteries (OR = 12.67; 95% CI: 1.41–113.84), lupus nephritis (OR = 3.69; 95% CI: 1.16–12.22), and obesity (OR = 4.21; 95% CI: 1.40–12.67). Autoantibodies related to IL-23 were anti-phosphatidylethanolamine antibodies (OR = 11.06; 95% CI: 1.24–98.65) and anti-SS-B/La antibodies (OR = 15.43; 95% CI: 1.73–137.25). Conclusions IL-23 may be involved in lupus nephritis pathogenesis. Through its association with obesity and selected antiphospholipid antibodies, IL-23 might promote a hypercoagulable state contributing to atherothrombosis development in SLE patients.

Highlights

  • Systemic lupus erythematosus (SLE) is a chronic, inflammatory, multisystem autoimmune disease characterized by an irreversible break in immunologic self-tolerance and successive immune-mediated tissue damage [1]

  • Various immunosuppressive therapeutic schemes were applied in the patients and the majority of them went into remission which might be the case of antinuclear antibodies (ANA) disappearance in some of the SLE patients

  • We evaluated the relationship between serum levels of IL-23 and clinical and laboratory characteristics of SLE with the special focus on atherosclerosis and atherosclerotic risk factors

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Summary

Introduction

Systemic lupus erythematosus (SLE) is a chronic, inflammatory, multisystem autoimmune disease characterized by an irreversible break in immunologic self-tolerance and successive immune-mediated tissue damage [1]. The crucial role in SLE pathogenesis plays innate and adaptive immune dysregulation, and it has been confirmed that certain cytokines are closely linked to SLE pathogenesis [6]. IL-23 is produced by macrophages, dendritic cells, keratinocytes, and other antigen-presenting cells and through its Mediators of Inflammation interaction with the IL-23 receptor plays a central role in inflammation including the induction of Th17 cells [8, 9]. The IL-23-IL-17 axis is emerging as a critical regulatory system that bridges the innate and adaptive arms of the immune system and plays a critical role in development of autoimmune inflammatory diseases [10]. IL-23 has been implicated in SLE [17,18,19,20], atherosclerosis [21, 22], and obesity [23]

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