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[The roles of IL-17 and CXCR4 in chronic allograft nephropathy in rat models]

W Wang1, Y Xu, W J Jiao

  • 1Department of Urology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.

Zhonghua Yi Xue Za Zhi
|February 13, 2018
PubMed

Insights

Interleukin-17 (IL-17) and its receptor CXCR4 play a role in chronic graft nephropathy (CAN). Increased Th17 cells and IL-17 expression in CAN rat models suggest SDF-1/CXCR4 may attract these cells, promoting kidney damage.

Area of Science:

  • Immunology
  • Nephrology
  • Transplantation Biology

Background:

  • Chronic graft nephropathy (CAN) is a major cause of kidney transplant failure.
  • The precise mechanisms underlying CAN progression remain incompletely understood.
  • Identifying key molecular players is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the involvement and mechanism of Interleukin-17 (IL-17) and its receptor CXCR4 in the development of CAN.
  • To elucidate the potential role of the SDF-1/CXCR4 axis in recruiting immune cells to the injured kidney.

Main Methods:

  • Establishment of a rat model for CAN using Fisher 344 to Lewis rat transplants.
  • Pathological examination of renal allografts to assess injury.
  • Quantification of SDF-1/CXCR4, IL-17, and α-SMA expression via immunohistochemistry and ELISA.
  • Flow cytometry analysis of CD4+, CXCR4+, and IL-17+ cells, specifically Th17 cells.

Main Results:

  • CAN rat models exhibited significant pathological damage compared to controls.
  • Elevated serum and renal expression of SDF-1/CXCR4 and IL-17 were observed in CAN rats.
  • A notable increase in Th17 cell counts and IL-17 levels was detected in both blood and kidneys of CAN rats.

Conclusions:

  • Th17 cell infiltration and elevated IL-17 levels are characteristic of the CAN rat model.
  • The SDF-1/CXCR4 signaling pathway may mediate the chemotaxis of Th17 cells to the injured kidney.
  • IL-17 expression might contribute to renal cell transformation into fibroblasts, driving CAN progression.
Keywords:
CXCR4 receptorsInterleukin-17Renal transplantation

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