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04 October 2016 : Original article  

The Potential Role of IL-33 in Renal Transplant Recipients with Chronic Allograft Dysfunction

Jiexiu ZhangEF, Zijie WangA, Zhen XuCD, Zhijian HanE, Jun TaoBC, Pei LuB, Zhengkai HuangD, Wanli ZhouD, Chunchun ZhaoF, Ruoyun TanA, Min GuAG

DOI: 10.12659/AOT.899263

Ann Transplant 2016; 21:611-618

Abstract

BACKGROUND: 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

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Annals of Transplantation eISSN: 2329-0358
Annals of Transplantation eISSN: 2329-0358