Evidence map›Paper›PMID 38504554›Full record

ArticleClinical and translational medicine2024

Interleukin-2/anti-interleukin-2 immune complex attenuates cold ischemia-reperfusion injury after kidney transplantation by increasing renal regulatory T cells.

Joon Young Jang, Hyung Woo Kim, Ji-Jing Yan, Tae Kyeom Kang, Wook-Bin Lee, Beom Seok Kim, Jaeseok Yang

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Machine Perfusion and Bioengineering Strategies in Transplantation-Beyond the Emerging Concepts.Transplant international : official journal of the European Society for Organ Transplantation · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Joon Young JangDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hyung Woo KimDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-6305-452X
Ji-Jing YanDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.
Tae Kyeom KangNatural Product Research Center, Korea Institute of Science and Technology, Gangneung, Republic of Korea.
Wook-Bin LeeNatural Product Research Center, Korea Institute of Science and Technology, Gangneung, Republic of Korea.
Beom Seok KimDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-5732-2583
Jaeseok YangDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-5378-7797
Yonsei University · KRKorea Institute of Science and Technology · KR

Funding

Ministry of Science and ICT NRF-2018R1A2B3001179Ministry of Science and ICT NRF-2022R1A2C3003496
6 · The paper itself

Abstract

backgroundCold 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.

methodsWe developed a cold IRI mouse model using kidney transplantation and analyzed the IL-2C impact on cold IRI in acute, subacute and chronic phases.

resultsTreg 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.

conclusionTregs 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. KEY POINTS: Interleukin (IL)-2/anti-IL-2 antibody complex attenuated acute renal injury, facilitated subacute renal regeneration and suppressed chronic renal fibrosis after cold ischemia-reperfusion injury (IRI) by increasing the renal Tregs. IL-2/anti-IL-2 antibody complex decreased reactive oxygen species-mediated injury and improved antioxidant function. This study suggests the therapeutic potential of the IL-2/anti-IL-2 antibody complex in kidney transplantation-associated cold IR.

Indexed as

Acute Kidney InjuryKidney TransplantationReperfusion InjuryAnimalsAntigen-Antibody ComplexAntioxidantsFibrosisInterleukin-2KidneyMiceReactive Oxygen SpeciesT-Lymphocytes, RegulatoryAntigen-Antibody ComplexAntioxidantsInterleukin-2Reactive Oxygen Speciescold ischemia-reperfusion injuryIL-2/anti-IL-2 immune complexkidney transplantationregulatory T cells

Identifiers

PMID38504554
PMCPMC10951489
OpenAlexW4393010801

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.