Dysregulated expression of interleukin-23 and interleukin-12 subunits in systemic lupus erythematosus patients
Xinfang Huang, Jing Hua, Nan Shen, Shun‐le Chen
Abstract
Xinfang Huang, Jing Hua, Nan Shen, Shun‐le Chen
Abstract
The aim of this study was to investigate the regulation of interleukin (IL)-12 and IL-23 expression in the autoimmune disease, systemic lupus erythematosus (SLE). mRNA from healthy subjects and SLE patients were prepared from peripheral blood mononuclear cells (PBMC) and quantitative real-time polymerase chain reaction was performed to quantify IL-23 specific subunit P19, IL-12 specific subunit P35, and their common subunit P40. IL-12 specific subunit P35 mRNA expression in untreated and treated SLE patients was significantly lower than healthy controls (P = 0.015 and 0.000, respectively). Compared with untreated SLE patients, treatment of SLE patients with corticosteroids or corticosteroids plus another immunosuppressor significantly suppressed P40 and P19 expression (P = 0.002 and 0.015, respectively). The mRNA levels of p19, p40, and p35 in active SLE patients (SLEDAT > 10) were significantly higher compared with those in the inactive SLE patients (SLEDAI ≤ 10) (P = 0.000, 0.000, and 0.017, respectively). These results suggest that deficiency of IL-12 and possibly upregulation of IL-23 may contribute to SLE pathogenesis and both cytokines may be therapeutic targets in SLE.
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The aim of this study was to investigate the regulation of interleukin (IL)-12 and IL-23 expression in the autoimmune disease, systemic lupus erythematosus (SLE). mRNA from healthy subjects and SLE patients were prepared from peripheral blood mononuclear cells (PBMC) and quantitative real-time polymerase chain reaction was performed to quantify IL-23 specific subunit P19, IL-12 specific subunit P35, and their common subunit P40. IL-12 specific subunit P35 mRNA expression in untreated and treated SLE patients was significantly lower than healthy controls (P = 0.015 and 0.000, respectively). Compared with untreated SLE patients, treatment of SLE patients with corticosteroids or corticosteroids plus another immunosuppressor significantly suppressed P40 and P19 expression (P = 0.002 and 0.015, respectively). The mRNA levels of p19, p40, and p35 in active SLE patients (SLEDAT > 10) were significantly higher compared with those in the inactive SLE patients (SLEDAI ≤ 10) (P = 0.000, 0.000, and 0.017, respectively). These results suggest that deficiency of IL-12 and possibly upregulation of IL-23 may contribute to SLE pathogenesis and both cytokines may be therapeutic targets in SLE.
Key concepts: Medicine, Peripheral blood mononuclear cell, Pathogenesis, Interleukin 23, Immunology, Lupus erythematosus, Interleukin, Rheumatology