ReviewInternational journal of molecular sciences2019
Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Immune cells during compensatory renal hypertrophy after unilateral nephrectomy.Research square · 2026Article
- Immunological mechanisms and novel therapeutic strategies for sepsis‑associated acute kidney injury (Review).International journal of molecular medicine · 2026Review
- Causal association between circulating blood cell traits and pulmonary embolism: a mendelian randomization study.Thrombosis journal · 2024Article
- Multi-Omic Analysis Reveals Genetic Determinants and Therapeutic Targets of Chronic Kidney Disease and Kidney Function.International journal of molecular sciences · 2024Article
- Machine learning-based identification of novel hub genes associated with oxidative stress in lupus nephritis: implications for diagnosis and therapeutic targets.Lupus science & medicine · 2024Article
- Article
- Involvement of Innate Immune System in the Pathogenesis of Sepsis-Associated Acute Kidney Injury.International journal of molecular sciences · 2023Article
- Heatstroke-induced acute kidney injury and the innate immune system.Frontiers in medicine · 2023Review
- Review
- Identification of blood-based key biomarker and immune infiltration in Immunoglobulin A nephropathy by comprehensive bioinformatics analysis and a cohort validation.Journal of translational medicine · 2022Article
- Infections, Reactions of Natural Killer T Cells and Natural Killer Cells, and Kidney Injury.International journal of molecular sciences · 2022Review
- Identification of novel key genes and potential candidate small molecule drugs in diabetic kidney disease using comprehensive bioinformatics analysis.Frontiers in genetics · 2022Article
- The role of tumor necrosis factor in triggering activation of natural killer cell, multi-organ mitochondrial dysfunction and hypertension during pregnancy.Pregnancy hypertension · 2021Article
- Knockdown of circ-FANCA alleviates LPS-induced HK2 cell injury via targeting miR-93-5p/OXSR1 axis in septic acute kidney injury.Diabetology & metabolic syndrome · 2021Article
- Friends or foes? The knowns and unknowns of natural killer cell biology in COVID-19 and other coronaviruses in July 2020.PLoS pathogens · 2020Review
- Neuroimmune Mechanisms in Signaling of Pain During Acute Kidney Injury (AKI).Frontiers in medicine · 2020Review
- Protopine Protects Mice against LPS-Induced Acute Kidney Injury by Inhibiting Apoptosis and Inflammation via the TLR4 Signaling Pathway.Molecules (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse natural killer T (NKT) cells and natural killer (NK) cells are innate immune cells that are highly abundant in the liver. In addition to their already-known antitumor and antimicrobial functions, their pathophysiological roles in the kidney have recently become evident. Under normal circumstances, the proportion of activated NKT cells in the kidney increases with age. Administration of a synthetic sphingoglycolipid ligand (alpha-galactosylceramide) further activates NKT cells, resulting in injury to renal vascular endothelial cells via the perforin-mediated pathway and tubular epithelial cells via the TNF-α/Fas ligand pathway, causing acute kidney injury (AKI) with hematuria. Activation of NKT cells by common bacterial DNA (CpG-ODN) also causes AKI. In addition, NKT cells together with B cells play significant roles in experimental lupus nephritis in NZB/NZW F1 mice through their Th2 immune responses. Mouse NK cells are also assumed to be involved in various renal diseases, and there may be complementary roles shared between NKT and NK cells. Human CD56
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Registered trials
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.