ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Both PD-1 ligands protect the kidney from ischemia reperfusion injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 85 citations in OpenAlex.
- T Cell-Independent Role of PD-L1 in Kidney Repair: Mitigation of Tubular DNA Damage via PD-L1/BRCA1 Interaction Following AKI.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Resident Macrophage-Orchestrated Immune and Fibroblast Interactions in Immune Checkpoint Inhibitor-Associated Nephrotoxicity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Acute kidney injury: pathogenesis and therapeutic interventions.Molecular biomedicine · 2025Review
- Longitudinal serum proteomics identifies inflammatory and metabolic pathways in hypertensive nephrosclerosis progression.Clinical proteomics · 2025Article
- Advances in Nano-Immunomodulatory Systems for the Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Targeting Inflammatory Imbalance in Chronic Kidney Disease: Focus on Anti-Inflammatory and Resolution Mediators.International journal of molecular sciences · 2025Review
- From chronic inflammation to immune escape: mapping the tumor microenvironment evolution in renal cell carcinoma.Frontiers in immunology · 2025Review
- Enhanced renal ischemia/reperfusion injury repair potential of exosomes derived from B7-H1Frontiers in genetics · 2025Article
- The immune regulatory role of lymphangiogenesis in kidney disease.Journal of translational medicine · 2024Review
- Double-negative T cells have a reparative role after experimental severe ischemic acute kidney injury.American journal of physiology. Renal physiology · 2024Article
- All-cause and immune checkpoint inhibitor-associated acute kidney injury in immune checkpoint inhibitor users: a meta-analysis of occurrence rate, risk factors and mortality.Clinical kidney journal · 2024Article
- Nephrotoxicity in the Age of Immune Checkpoint Inhibitors: Mechanisms, Diagnosis, and Management.International journal of molecular sciences · 2023Review
- Recruitment of myeloid‑derived suppressor cells and regulatory T‑cells is associated with the occurrence of acute myocardial infarction.Biomedical reports · 2023Article
- Single-cell transcriptomics reveal a hyperacute cytokine and immune checkpoint axis after cardiac arrest in patients with poor neurological outcome.Med (New York, N.Y.) · 2023Article
- Neoadjuvant transarterial chemoembolization (TACE) plus PD-1 inhibitor bridging to tumor resection in intermediate-stage hepatocellular carcinoma patients.Irish journal of medical science · 2023Article
- Targeting PD-1/PD-L1 inhibits rejection in a heterotopic tracheal allograft model of lung transplantation.Frontiers in pharmacology · 2023Article
- Immune-related adverse events of immune checkpoint inhibitors: a review.Frontiers in immunology · 2023Review
- Diagnosis and management of immune checkpoint inhibitor-associated acute kidney injury.Nature reviews. Nephrology · 2022Review
- The Programmed Death-1 Signaling Axis Modulates Inflammation and LV Structure/Function in a Stress-Induced Cardiomyopathy Model.JACC. Basic to translational science · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is a common problem in hospitalized patients that enhances morbidity and mortality and promotes the development of chronic and end-stage renal disease. Ischemia reperfusion injury (IRI) is one of the major causes of AKI and is characterized by uncontrolled renal inflammation and tubular epithelial cell death. Our recent studies demonstrated that regulatory T cells (Tregs) protect the kidney from ischemia reperfusion-induced inflammation and injury. Blockade of programmed death-1 (PD-1) on the surface of Tregs, prior to adoptive transfer, negates their ability to protect against ischemic kidney injury. The present study was designed to investigate the role of the known PD-1 ligands, PD-L1 and PD-L2, in kidney IRI. Administration of PD-L1 or PD-L2 blocking Abs prior to mild or moderate kidney IRI significantly exacerbated the loss of renal function, renal inflammation, and acute tubular necrosis compared with mice receiving isotype control Abs. Interestingly, blockade of both PD-1 ligands resulted in worse injury, dysfunction, and inflammation than did blocking either ligand alone. Genetic deficiency of either PD-1 ligand also exacerbated kidney dysfunction and acute tubular necrosis after subthreshold ischemia. Bone marrow chimeric studies revealed that PD-L1 expressed on non-bone marrow-derived cells is critical for this resistance to IRI. Finally, blockade of either PD-1 ligand negated the protective ability of adoptively transferred Tregs in IRI. These findings suggest that PD-L1 and PD-L2 are nonredundant aspects of the natural protective response to ischemic injury and may be novel therapeutic targets for AKI.
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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 OpenQuestion graph.