ArticleJournal of the American Society of Nephrology : JASN2008
NKT cells inhibit the development of experimental crescentic glomerulonephritis.
Article in Journal of the American Society of Nephrology : JASN, 2008. 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, 25 citations in OpenAlex.
- IFN-γ-dominant immune shift is associated with reduced protective ILC2 responses in chronic kidney disease.Frontiers in immunology · 2026Article
- Advancements in understanding and treating CXCL16/CXCR6 in tumors and in inflammatory diseases: a narrative review.Frontiers in immunology · 2026Review
- The role of CXCL16 in atherosclerosis: from mechanisms to therapy.Frontiers in immunology · 2025Review
- Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022Review
- Unconventional T cells and kidney disease.Nature reviews. Nephrology · 2021Review
- Retroviral Transduction of NKT Hybridoma Cells.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Splenocyte transfer exacerbates salt-sensitive hypertension in rats.Experimental physiology · 2020Article
- Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury.International journal of molecular sciences · 2019Review
- Tissue-Resident Lymphocytes in the Kidney.Journal of the American Society of Nephrology : JASN · 2018Review
- Murine DX5Journal of immunology research · 2018Article
- NKT cell modulates NAFLD potentiation of metabolic oxidative stress-induced mesangial cell activation and proximal tubular toxicity.American journal of physiology. Renal physiology · 2016Article
- Invariant natural killer T cells are depleted in renal impairment and recover after kidney transplantation.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2014Article
- Immature renal dendritic cells recruit regulatory CXCR6(+) invariant natural killer T cells to attenuate crescentic GN.Journal of the American Society of Nephrology : JASN · 2012Article
- Sulfatide-reactive natural killer T cells abrogate ischemia-reperfusion injury.Journal of the American Society of Nephrology : JASN · 2011Article
- Spontaneous focal activation of invariant natural killer T (iNKT) cells in mouse liver and kidney.BMC biology · 2010Article
- Neutralizing endogenous chemokines with small molecules. Principles and potential therapeutic applications.Pharmacology & therapeutics · 2010Review
- Invariant natural killer T cells and TGF-beta attenuate anti-GBM glomerulonephritis.Journal of the American Society of Nephrology : JASN · 2009Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD1d is an MHC class I-like, beta2-microglobulin-associated protein, constitutively expressed by antigen-presenting cells and some epithelial cells, which is recognized by NKT cells, a subpopulation of T cells. CD1d-dependent NKT cells confer protection in immune-mediated disorders, but whether these cells modulate the development of glomerulonephritis is unknown. Experimental crescentic glomerulonephritis was induced by administering anti-glomerular basement membrane antibodies to NKT cell-deficient (CD1d(-/-)) and wild-type mice. Compared with wild-type mice, NKT cell-deficient mice had an accelerated course of glomerulonephritis measured by renal function and crescent formation, and this was abrogated by adoptive transfer of NKT cells. Reconstitution with NKT cells also attenuated intraglomerular expression of TGF-beta1 and decreased phosphorylation of the transcription factors NF-kappaB and IkappaB. Adopted transfer of fluorescence-labeled NKT cells demonstrated their distribution to glomeruli damaged by anti-glomerular basement membrane antibodies but not to the tubulointerstitium. The chemokine CXCL16, which is the ligand for CXCR6 on NKT cells, was upregulated in glomeruli after induction of glomerulonephritis, and NKT cells were present in the same glomeruli. In vitro, NKT cells inhibited LPS-stimulated proliferation of mesangial cells, an affect that was reduced by co-current treatment with an anti-CXCL16 monoclonal antibody. In summary, these findings highlight the regulatory capacity of CD1d-dependent NKT cells in experimental glomerulonephritis and suggest that CXCL16 is involved in the recruitment of these cells to the site of injury.
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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.