한빛사논문
- 조회503
Joon Young Jang 1, Hyung Woo Kim 1, Ji-Jing Yan 1, Tae Kyeom Kang 2, Wook-Bin Lee 2, Beom Seok Kim 1, Jaeseok Yang 1
1Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.
2Natural Product Research Center, Korea Institute of Science and Technology, Gangneung, Republic of Korea.
Joon Young Jang, Hyung Woo Kim and Ji-Jing Yan equally contributed to this work.
Correspondence : Jaeseok Yang
Abstract
Background: Cold ischemia-reperfusion injury (IRI) is an unavoidable complication of kidney transplantation. We investigated the role of regulatory T cells (Treg) in cold IRI and whether the interleukin (IL)-2/anti-IL-2 antibody complex (IL-2C) can ameliorate cold IRI.
Methods: We developed a cold IRI mouse model using kidney transplantation and analyzed the IL-2C impact on cold IRI in acute, subacute and chronic phases.
Results: Treg transfer attenuated cold IRI, while Treg depletion aggravated cold IRI. Next, IL-2C administration prior to IRI mitigated acute renal function decline, renal tissue damage and apoptosis and inhibited infiltration of effector cells into kidneys and pro-inflammatory cytokine expression on day 1 after IRI. On day 7 after IRI, IL-2C promoted renal regeneration and reduced subacute renal damage. Furthermore, on day 28 following IRI, IL-2C inhibited chronic fibrosis. IL-2C decreased reactive oxygen species-mediated injury and improved antioxidant function. When IL-2C was administered following IRI, it also increased renal regeneration with Treg infiltration and suppressed renal fibrosis. In contrast, Treg depletion in the presence of IL-2C eliminated the positive effects of IL-2C on IRI.
Conclusion: Tregs protect kidneys from cold IRI and IL-2C inhibited cold IRI by increasing the renal Tregs, suggesting a potential of IL-2C in treating cold IRI.
논문정보
- Research article
- 2024년 03월 (BRIC 등록일 2024-04-02)
- 국내 연구진
- 의약학 > 응용의학
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