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

Ann Transplant. 2016 Oct 4:21:611-618. doi: 10.12659/aot.899263.

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.

MeSH terms

  • Adult
  • Case-Control Studies
  • Cytokines / blood
  • Female
  • Graft Rejection / blood
  • Graft Rejection / etiology*
  • Graft Rejection / immunology*
  • Graft Survival / immunology
  • Humans
  • Interleukin-33 / blood*
  • Kidney Transplantation / adverse effects*
  • Male
  • Middle Aged
  • T-Lymphocyte Subsets / immunology

Substances

  • Cytokines
  • IL33 protein, human
  • Interleukin-33