ArticleMediators of inflammation2015
Protective Effect of CXCR3⁺CD4⁺CD25⁺Foxp3⁺ Regulatory T Cells in Renal Ischemia-Reperfusion Injury.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Protective Arm of Renin-Angiotensin System: Evidence of Nephroprotective Effects Against Acute Kidney Injury.Acta physiologica (Oxford, England) · 2026Review
- Engineered extracellular vesicles promote the repair of acute kidney injury by modulating regulatory T cells and the immune microenvironment.Journal of translational medicine · 2025Article
- The emerging role of tissue regulatory T cells in tissue repair and regeneration.Frontiers in immunology · 2025Review
- IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells.Cellular and molecular life sciences : CMLS · 2023Article
- Revisiting regulatory T cells as modulators of innate immune response and inflammatory diseases.Frontiers in immunology · 2023Review
- CD4Frontiers in immunology · 2023Review
- CXCR3 alleviates renal ischemia‑reperfusion injury via increase of Tregs.Molecular medicine reports · 2021Article
- Angiotensin type 2 receptor activation limits kidney injury during the early phase and induces Treg cells during the late phase of renal ischemia.American journal of physiology. Renal physiology · 2021Article
- Molecular Aspects of Volatile Anesthetic-Induced Organ Protection and Its Potential in Kidney Transplantation.International journal of molecular sciences · 2021Review
- Mesenchymal Stem Cell Protects Injured Renal Tubular Epithelial Cells by Regulating mTOR-Mediated Th17/Treg Axis.Frontiers in immunology · 2021Review
- Effect of infusion of M&G solution for protection of renal tissue in Wistar rats subjected to programmed ischemia-reperfusion.Jornal vascular brasileiro · 2020Article
- Losartan accelerates the repair process of renal fibrosis in UUO mouse after the surgical recanalization by upregulating the expression of Tregs.International urology and nephrology · 2019Article
- A modified relief of unilateral ureteral obstruction model.Renal failure · 2019Article
- Regulatory T cells in renal disease.Clinical & translational immunology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulatory T cells (Tregs) suppress excessive immune responses and are potential therapeutic targets in autoimmune disease and organ transplantation rejection. However, their role in renal ischemia-reperfusion injury (IRI) is unclear. Levels of Tregs and expression of CXCR3 in Tregs were analyzed to investigate their function in the early phase of renal IRI. Mice were randomly divided into Sham, IRI, and anti-CD25 (PC61) + IRI groups. The PC61 + IRI group was established by i.p. injection of PC61 monoclonal antibody (mAb) to deplete Tregs before renal ischemia. CD4(+)CD25(+)Foxp3(+) Tregs and CXCR3 on Tregs were analyzed by flow cytometry. Blood urea nitrogen (BUN), serum creatinine (Scr) levels, and tubular necrosis scores, all measures of kidney injury, were greater in the IRI group than in the Sham group. Numbers of Tregs were increased at 72 h after reperfusion in kidney. PC61 mAb preconditioning decreased the numbers of Tregs and aggravated kidney injury. There was no expression of CXCR3 on Tregs in normal kidney, while it expanded at 72 h after reperfusion and inversely correlated with BUN, Scr, and kidney histology score. This indicated that recruitment of Tregs into the kidney was related to the recovery of renal function after IRI and CXCR3 might be involved in the migration of Tregs.
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