The Potential Role of IL-33/ST2 Pathway in Renal Allograft Rejection
1Hanyang University Guri Hospital, Guri, Korea, Republic of, 2Seoul National University Hospital, Seoul, Korea, Republic of, 3Cheju Halla General Hospital, Jeju, Korea, Republic of
Meeting: 2019 American Transplant Congress
Abstract number: C31
Keywords: Kidney transplantation, Rejection, Screening
Session Information
Session Name: Poster Session C: Innate Immunity; Chemokines, Cytokines, Complement
Session Type: Poster Session
Date: Monday, June 3, 2019
Session Time: 6:00pm-7:00pm
Presentation Time: 6:00pm-7:00pm
Location: Hall C & D
*Purpose: 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. We hypothesized that IL-33 and ST2 expression differently express according to rejection type in renal allograft rejection.
*Methods: 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 were performed. We also evaluated the change of expression of IL-33/ST2 in dose of the anti ST2 Ab (0.5 μg/ml and 1 μg/ml).
*Results: In comparison with the EILSA, 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 was also decreased after treatment with anti ST2 Ab by each group. Anti ST2 Ab caused a decrease in mixed lymphocyte reaction and IL-8. The decrease was statistically significant at high concentrations. We found that anti ST2 Ab was able to significantly decrease chemotaxis.
*Conclusions: Expression 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.
To cite this abstract in AMA style:
Yu M, Kim Y, Moon J, Lee S, Lee H, Kim D, Lee C, Kim Y, Yang S. The Potential Role of IL-33/ST2 Pathway in Renal Allograft Rejection [abstract]. Am J Transplant. 2019; 19 (suppl 3). https://atcmeetingabstracts.com/abstract/the-potential-role-of-il-33-st2-pathway-in-renal-allograft-rejection/. Accessed May 11, 2025.« Back to 2019 American Transplant Congress