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Updated: Feb 4, 2026

Expression of Exogenous Cytokine in Patient-derived Xenografts via Injection with a Cytokine-transduced Stromal Cell Line
Published on: May 10, 2017
Induction therapy downregulates the expression of Th17/Tfh cytokines in patients with active lupus nephritis
Na Wang1, Congcong Gao1, Siwan Cui1
1The First Affiliated Hospital of Zhengzhou University Rheumatology, No. 1 Jianshe Road, Zhengzhou, Henan Province, People's Republic of China.
Abstract:
To determine the potential changes of IL-6, IL-17A and IL-21 levels during induction therapy, and to assess their relationship with disease activity and immunologic features on patients with active lupus nephritis, twenty-eight patients treated with corticosteroid and immunosuppressants were included in this study. Demographic, clinical, serological data and disease activity were assessed. Blood samples were collected at week 0, 12 and 24, and serum concentrations of IL-17A, IL-6 and IL-21 were measured by cytometric bead array. The serum concentrations of IL-6, IL-17A and IL-21 (P<0.001, P<0.01, P=0.001, respectively) decreased progressively during induction therapy. Concentration of IL-6, IL-17A and IL-21 was higher in non-remission group than that in remission group. A positive correlation was established between the concentration of these cytokines and the severity of proteinuria (P<0.001, P=0.020, P=0.045, respectively), ESR (P<0.001), SLEDAI scores (P<0.05), and ANA titers (P=0.018, P=0.048, P<0.05, respectively). Additionally, ROC curve analysis for IL-6, IL-17A and IL-21 was performed to predict the disease activity. The optimal cutoff level was 5.78 pg/ml, 1.98 pg/ml and 8.59 pg/ml, with AUC=0.809, 0.735 and 0.786. The concentration of IL-6 and IL-21 may be regarded as an indicator for the remission of active lupus nephritis, with cutoff value of 9.12 pg/ml and 11.30 pg/ml, while AUC=0.930 and 0.896. The production of serum IL-6, IL-17A and IL-21 in active LN was dramatically declined during induction therapy, which may improve disease activity while delay disease progression of LN.
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