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Abstract: FR-PO849

The Potential Role of IL-33/ST2 Pathway in Renal Allograft Rejection

Session Information

  • Transplantation: Basic
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Transplantation

  • 1801 Transplantation: Basic


  • Yu, Mi-yeon, Seoul national university hospital, Seoul, Korea (the Republic of)
  • Lee, Jae Wook, National Cancer Center, Seoul, Korea (the Republic of)
  • Kim, Yong Chul, Seoul National University Hospital, Jongno-gu, Seoul, Korea (the Republic of)
  • Lee, Sunhwa, Seoul National University Hospital, Jongno-gu, Seoul, Korea (the Republic of)
  • Jeon, Un Sil, Sheikh Khalifa Specialty Hospital, Ras Al Khaimah, United Arab Emirates
  • Lee, Hajeong, Seoul National University College of Medicine, Seoul, Korea (the Republic of)
  • Kim, Dong Ki, Seoul National University Hospital, Jongno-gu, Seoul, Korea (the Republic of)
  • Kim, Yon Su, Seoul National University College of Medicine, Seoul, Korea (the Republic of)
  • Yang, Seung Hee, Kidney Research Institute, Seoul National University, Seoul, Korea (the Republic of)

Interleukin (IL)-33 is one of IL-1 family cytokine that has pleiotropic effects, such as inflammation promotion and immune response regulation. Recent studies showed that IL-33 and its receptor, growth stimulation gene-2 (ST2) are biomarkers in heart allograft rejection. However, there is no studies about their role in renal allograft rejection. Moreover, its response according to rejection type remain unclear. We that IL-33 and ST2 expression differently express according to rejection type in renal allograft rejection.


Serum and kidney biopsy tissue were obtained from healthy controls and kidney transplanted recipients with acute antibody mediated rejection (AAMR), acute cell mediated rejection (ACMR), and chronic antibody mediated rejection (CAMR). We compared the expression of IL-33 and ST2 between 4 groups. To test the suppressive effect of anti-ST2 monoclonal antibody (anti-ST2 Ab), mixed lymphocyte reaction and chemotaxis assays by Boyden chambers were performed. We also evaluated the change of expression of IL-33/ST2 in dose of the anti-ST2 Ab (0.5 and 1 μg/ml).


In comparison with the ELISA, ST2 level was higher in rejection group than in control group. The level of IL-33 was too low to be analyzed. Immunohistochemical analysis demonstrated that IL-33 and ST2 elevate in kidney tissue with rejection, especially in acute rejection. However, the expressions of IL-33/ST2 were no difference between AAMR and ACMR. In response to anti-ST2 Ab, primary human renal proximal tubular epithelial cells, which was stimulated by recipients’ serum, showed a decrease in fibronectin and IL-33/ST2. IL-8, pro-inflammatory cytokine, was also decreased after treatment with anti-ST2 Ab by each group. In vitro validation, anti-ST2 Ab caused decreases in proliferation of lymphocyte and the level of IL-8. These decreases were significantly at high concentrations. We found that anti-ST2 Ab was able to significantly decrease chemotaxis.


Expressions of IL-33 and ST2 are higher in acute rejection than chronic rejection. Pro-inflammatory cytokines associate with IL-33/ST2 pathway during rejection. Blocking of the IL-33/ST2 axis may contribute to protect the allograft rejection.