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Year : 2014  |  Volume : 34  |  Issue : 2  |  Page : 120-125

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

1 Department of Dermatology and Venereology, Faculty of Medicine, Tanta University, Tanta, Egypt
2 Department of Dermatology and Venereology, Faculty of Medicine, Miser University for Science and Technology (MUST University), El-Giza, Egypt
3 Department of Clinical Pathology, Faculty of Medicine, Tanta University, Tanta, Egypt
4 Department of Internal Medicine, Faculty of Medicine, Tanta University, Tanta, Egypt
5 Department of Dermatology and Venereology, Ministry of Health, Tanta, Egypt

Correspondence Address:
Doaa Salah Hegab
MD, Department of Dermatology and Venereology, Faculty of Medicine, Tanta University Hospitals, El Geish Street, Tanta 31111
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1110-6530.150269

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Background Systemic 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. Aims This 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 methods Thirty-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. Results Serum 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. Conclusion Findings 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.

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