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DOI 10.30699/ijp.2025.2051460.3403

Медицинская библиотека · Iranian journal of pathology · 2025

IL-8/CD181 Mediated Inflammation in SLE-Associated Hemolytic Anemia.

Mohsin Muslim Idan, Al-Hilali Samer A Mh, Mohsin Rusul Idan, Mohasin Mohammed, Al-Shamarti Mohammed Jasim Mohammed

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Аннотация

BACKGROUND &

OBJECTIVE

Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by immune dysregulation, autoantibody production, and organ damage, notably in the kidneys. Cytokine imbalances contribute to SLE's diverse clinical presentations. This study investigated the roles of interleukin-8 (IL-8) and its receptor, CD181 (CXCR1), in SLE pathogenesis, specifically focusing on their association with hemolytic anemia, a severe complication.

METHODS

This research investigates the role of interleukin-8 (IL-8) and its cognate receptor, CXCR1 (CD181). It was analyzed clinical and demographic data from 250 SLE patients and quantified IL-8 and CD181 mRNA and protein expression in samples from patients with active SLE, inactive SLE, and SLE complicated by hemolytic anemia, comparing them to healthy controls.

RESULTS

Of the 250 samples, 84% were from SLE patients, with 67% in the active disease phase. Significant upregulation of both IL-8 and CD181 mRNA and protein was observed in SLE patients compared to controls. Specifically, mRNA expression was significantly elevated in active SLE (p=0.0001) and inactive SLE (p=0.01). Notably, IL-8 mRNA expression was significantly higher in SLE patients with hemolytic anemia (p<0.0001) compared to those without (p<0.01(.

CONCLUSION

These findings suggest that the IL-8/CD181 axis plays a crucial role in the inflammatory processes and tissue damage associated with SLE, particularly in the development of hemolytic anemia.

Для цитирования: Mohsin Muslim Idan, Al-Hilali Samer A Mh, Mohsin Rusul Idan, Mohasin Mohammed, Al-Shamarti Mohammed Jasim Mohammed. IL-8/CD181 Mediated Inflammation in SLE-Associated Hemolytic Anemia.. Iranian journal of pathology. 2025. DOI: 10.30699/ijp.2025.2051460.3403.
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