Interleukin-26 in Systemic Lupus Erythematosus: Demographic Correlates, Mechanistic Insights, and the Impact of Rituximab Therapy

Document Type : New and original researches in the field of Microbiology.

Authors

Department of Medical Microbiology, College of Medicine, University of Kufa

Abstract

Background: Systemic lupus erythematosus (SLE) is an autoimmune disorder predominantly affecting young to middle-aged females, with a complex and not yet fully elucidated immunopathogenesis. Recent studies have suggested that cytokines such as interleukin-26 (IL-26) might be involved in SLE-related immune processes. Objectives: This study aimed to characterize the demographic and clinical profiles of SLE patients, assess their treatment regimens, and compare IL-26 levels between SLE patients and healthy controls. Additionally, we evaluated whether Rituximab therapy might be associated with alterations in IL-26 expression. Methodology: A total of 126 participants, including SLE patients and matched healthy controls, were enrolled in the study. Demographic data, treatment histories, and IL-26 levels were collected and analyzed using appropriate non-parametric statistical tests to identify significant differences between groups. Results. Consistent with previous reports, the majority of SLE patients were female (96.8%) and primarily in the 21–40-year age range. While the sex distribution was similar between SLE cases and controls, a significant difference in age distribution was observed (p=0.027). Rituximab was the most commonly administered treatment (66.7%), followed by Cyclophosphamide (20.6%). IL-26 levels were significantly lower in SLE patients compared to controls (p < 0.001), suggesting a potential association between immunosuppressive therapy and cytokine modulation. Conclusion: Our study confirms the typical demographic profile of SLE and identifies a significant reduction in IL-26 levels in patients, which may be related to the effects of Rituximab therapy. These findings provide preliminary insights into the potential role of IL-26 in SLE; however, further studies are needed to better understand its clinical relevance and underlying mechanisms.

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