Journal
ANNALS OF TRANSPLANTATION
Volume 21, Issue -, Pages 611-618Publisher
INT SCIENTIFIC INFORMATION, INC
DOI: 10.12659/AOT.899263
Keywords
Fibrosis; Immunity, Cellular; Kidney Transplantation
Categories
Funding
- National Natural Science Foundation of China [81570676, 81100532, 81470981]
- Science and Education Health Project of Jiangsu Province for Important Talent [RC2011055]
- 333 High Level Talents Project in Jiangsu Province
- Jiangsu Province Six Talents Peak from Department of Human Resources, Social Security Office of Jiangsu Province of China [2010WSN-56, 2011-WS-033]
- General Program of Department of Health of Jiangsu Province of China [H2009907]
- Priority Academic Program Development of Jiangsu Higher Education Institutions [JX10231801]
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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/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-gamma). 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.
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