Role of interleukin-23 in the immunopathogenesis of systemic lupus erythematosus

Abstract

BackgroundSystemic lupus erythematosus (SLE) is a complex and multifactorial autoimmune disease. T-helper 17 (Th17) cells are essential modulators for propagation of immune response in several autoimmune diseases. Interleukin-23 (IL-23) is a proinflammatory mediator that is necessary for the development of T-cell-dependent inflammation. IL-23 is essential to expand and maintain Th17 cells. Increased amounts of IL-23 have been associated with several autoimmune diseases.AimsThis work aimed to study the alteration in the serum level of IL-23 in patients with SLE in comparison with healthy individuals, and to correlate its serum level with disease activity to speculate on its possible role in the pathogenesis of SLE.Participants and methodsThirty-four adult patients with SLE (31 women and three men) and 30 healthy age and sex-matched controls were included. SLE patients were divided according to SLE disease activity index (SLEDAI) into active and inactive groups. IL-23 serum level was determined for all patients and controls using a quantitative enzyme-linked immunosorbent assay.ResultsSerum IL-23 concentration was significantly elevated in SLE patients than in the healthy controls (P = 0.001), and it correlated significantly with disease activity (P = 0.001). The median serum IL-23 concentrations were significantly higher in active SLE patients with renal involvement.ConclusionFindings support the presence of an important role of IL-23 in the pathogenesis of SLE. Our results indicate a possible relationship between the elevated serum levels of IL-23 and SLE activity. Marked elevation might be a predictor of renal insult in active cases.