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Jiexiu Zhang, Zijie Wang, Zhen Xu, Zhijian Han, Jun Tao, Pei Lu, Zhengkai Huang, Wanli Zhou, Chunchun Zhao, Ruoyun Tan, Min Gu
(Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China (mainland))
Ann Transplant 2016; 21:611-618
Chronic allograft dysfunction (CAD) is the major factor endangering the long-term allograft survival in kidney transplantation. The mechanisms of CAD remain unclear.
MATERIAL AND METHODS: A total of 64 renal transplant recipients were enrolled in our study and divided into a stable group and CAD group according to their allograft function. A group of 32 normal controls (healthy volunteers) were also included. An ELISA was used to detect serum interleukin-33 (IL-33), IL-2, IL-4, IL-10, IL-17, and interferon-gamma (IFN-γ). Flow cytometry was performed to measure the percentage of CD3+CD4+ and CD3+CD8+ T cells in the peripheral blood from the three patient groups. The correlations among the study indexes were also analyzed using Pearson’s method.
RESULTS: Levels of serum IL-33 was significantly higher in CAD patients than recipients with stable allograft function. Moreover, serum IL-2, IL-4, and IL-10 also increased statistically in patients with CAD. In addition, significant differences were observed in CD4+ T cells and the ratio of CD4+ and CD8+ T cells between CAD and stable patients.
CONCLUSIONS: Serum upregulated IL-33 could contribute to the pathogenesis of CAD in kidney transplant recipients.
Keywords: Fibrosis, Immunity, Cellular, Kidney Transplantation