Farhad Seif, Karrar Hadi Kadhim, Milad Ahmadaghdami, Paria Bayati, Somayeh Sadani, Homa Davoodi, Ali Memarian, Somayeh Ghorbani, Yasser Bagheri
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引用次数: 0
Abstract
Dysregulation of immune cells and cytokines, particularly T helper 17 (Th17) cells and their associated cytokines, is implicated in the pathogenesis of both systemic lupus erythematosus (SLE) and chronic kidney disease (CKD). This study aimed to investigate the serum levels of Th17-related cytokines (interleukin [IL]-17A, IL-21, IL-22, and IL-23) in CKD patients with and without SLE and explore their potential role in disease progression. A total of 118 participants were included, comprising 78 patients with CKD (stages 3-5) and 40 healthy controls. Cytokine levels were measured using enzyme-linked immunosorbent assay kits. Patients with CKD exhibited significantly lower IL-21 levels and higher IL-22 and IL-17A levels compared with controls, while patients with end-stage renal disease showed elevated IL-21 and IL-23 levels. Among SLE-negative nephrotic patients, IL-23 and IL-17A were significantly upregulated, whereas SLE-positive nephrotic patients had increased IL-22 and IL-17A levels. In addition, IL-21 and IL-17A were significantly correlated in patients with CKD, suggesting a potential immunoregulatory interplay. These findings indicate that Th17-related cytokines are differentially expressed depending on CKD stage and SLE status, potentially influencing immune responses, inflammation, and kidney fibrosis. Understanding alterations of these cytokines may aid in identifying targeted therapeutic, particularly for patients with CKD at risk of SLE-related complications.
期刊介绍:
Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.