ArticleJournal of the American Society of Nephrology : JASN2011
Sulfatide-reactive natural killer T cells abrogate ischemia-reperfusion injury.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- The Effect of Interleukin-10 Immunotherapy on Renal Ischemia-Reperfusion Injury: A Systematic Review and Meta-Analysis of Preclinical Studies.International journal of molecular sciences · 2024Pooled it
- The role of persistent inflammation in failed recovery after perinatal brain injury: is resolution the cure?Journal of neuroinflammation · 2026Review
- Dynamic regulation and targeted intervention of neutrophils in hepatic ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Functional remodeling of iNKT cells by sulfatide-reactive type II NKT cells reprograms alveolar macrophages to alleviate lung ischemia-reperfusion injury.Communications biology · 2026Article
- Multifaceted mechanisms of unconventional T cells in ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- IFN-γ-dominant immune shift is associated with reduced protective ILC2 responses in chronic kidney disease.Frontiers in immunology · 2026Article
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Diverse NKT cells regulate early inflammation and neurological outcomes after cardiac arrest and resuscitation.Science translational medicine · 2024Article
- Lymphocytes and innate immune cells in acute kidney injury and repair.Nature reviews. Nephrology · 2024Review
- Advances in lung ischemia/reperfusion injury: unraveling the role of innate immunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Interleukin-2/anti-interleukin-2 immune complex attenuates cold ischemia-reperfusion injury after kidney transplantation by increasing renal regulatory T cells.Clinical and translational medicine · 2024Article
- Chronic brain damage in HIV-infected individuals under antiretroviral therapy is associated with viral reservoirs, sulfatide release, and compromised cell-to-cell communication.Cellular and molecular life sciences : CMLS · 2023Article
- Thermotropic Behavior and Structural Organization of C24:1 Sulfatide Dispersions and Its Mixtures with Cationic Bilayers.ACS omega · 2023Article
- Role of tRNA derived fragments in renal ischemia-reperfusion injury.Renal failure · 2022Article
- Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022Review
- Role of T cells in ischemic acute kidney injury and repair.The Korean journal of internal medicine · 2022Review
- Infections, Reactions of Natural Killer T Cells and Natural Killer Cells, and Kidney Injury.International journal of molecular sciences · 2022Review
- Unconventional T cells and kidney disease.Nature reviews. Nephrology · 2021Review
- The role of lymphocytes in neonatal encephalopathy.Brain, behavior, & immunity - health · 2021Review
- Current status of research on exosomes in general, and for the diagnosis and treatment of kidney cancer in particular.Journal of experimental & clinical cancer research : CR · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is a significant immune response to ischemia-reperfusion injury (IRI), but the role of immunomodulatory natural killer T (NKT) cell subtypes is not well understood. Here, we compared the severity of IRI in mice deficient in type I/II NKT cells (CD1d(-/-)) or type I NKT cells (Jα18(-/-)). The absence of NKT cells, especially type II NKT cells, accentuated the severity of renal injury, whereas repletion of NKT cells attenuated injury. Adoptively transferred NKT cells trafficked into the tubulointerstitium, which is the primary area of injury. Sulfatide-induced activation of type II NKT cells protected kidneys from IRI, but inhibition of NKT cell recruitment enhanced injury. In co-culture experiments, sulfatide-induced activation of NKT cells from either mice or humans attenuated apoptosis of renal tubular cells after transient hypoxia via hypoxia-inducible factor (HIF)-1α and IL-10 pathways. Renal tissue of patients with acute tubular necrosis (ATN) frequently contained NKT cells, and the number of these cells tended to negatively correlate with ATN severity. In summary, sulfatide-reactive type II NKT cells are renoprotective in IRI, suggesting that pharmacologic modulation of NKT cells may protect against ischemic injury.
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