{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["20(6)"],"submitter":["Mesnard L"],"pubmed_abstract":["Invariant natural killer T (iNKT) cells represent a particular subset of T lymphocytes capable of producing several cytokines, which exert regulatory or effector functions, following stimulation of the T cell receptor. In this study, we investigated the influence of iNKT cells on the development of experimental anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). After injection of anti-GBM serum, the number of kidney iNKT cells rapidly increased. iNKT cell-deficient mice (Jalpha18-/-) injected with anti-GBM serum demonstrated worse renal function, increased proteinuria, and greater glomerular and tubular injury compared with similarly treated wild-type mice. We did not detect significant differences in Th1/Th2 polarization in renal tissue that might have explained the severity of disease in Jalpha18-/- mice. Interestingly, expression of both TGF-beta and TGF-beta-induced (TGFBI) mRNA was higher in wild-type kidneys compared with Jalpha18-/- kidneys, suggesting a possible protective role for TGF-beta in anti-GBM GN. Administration of an anti-TGF-beta neutralizing antibody significantly enhanced the severity of disease in wild-type, but not Jalpha18-/-, mice. In conclusion, in experimental anti-GBM GN, iNKT cells attenuate disease severity and TGF-beta has a renoprotective role."],"journal":["Journal of the American Society of Nephrology : JASN"],"pagination":["1282-92"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2689902"],"repository":["biostudies-literature"],"pubmed_title":["Invariant natural killer T cells and TGF-beta attenuate anti-GBM glomerulonephritis."],"pmcid":["PMC2689902"],"pubmed_authors":["Tillet Y","Vandermeersch S","Mesnard L","Michel ML","Rondeau E","Keller AC","Leite-de-Moraes MC","Rafat C","Letavernier E"],"additional_accession":[]},"is_claimable":false,"name":"Invariant natural killer T cells and TGF-beta attenuate anti-GBM glomerulonephritis.","description":"Invariant natural killer T (iNKT) cells represent a particular subset of T lymphocytes capable of producing several cytokines, which exert regulatory or effector functions, following stimulation of the T cell receptor. In this study, we investigated the influence of iNKT cells on the development of experimental anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). After injection of anti-GBM serum, the number of kidney iNKT cells rapidly increased. iNKT cell-deficient mice (Jalpha18-/-) injected with anti-GBM serum demonstrated worse renal function, increased proteinuria, and greater glomerular and tubular injury compared with similarly treated wild-type mice. We did not detect significant differences in Th1/Th2 polarization in renal tissue that might have explained the severity of disease in Jalpha18-/- mice. Interestingly, expression of both TGF-beta and TGF-beta-induced (TGFBI) mRNA was higher in wild-type kidneys compared with Jalpha18-/- kidneys, suggesting a possible protective role for TGF-beta in anti-GBM GN. Administration of an anti-TGF-beta neutralizing antibody significantly enhanced the severity of disease in wild-type, but not Jalpha18-/-, mice. In conclusion, in experimental anti-GBM GN, iNKT cells attenuate disease severity and TGF-beta has a renoprotective role.","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Jun","modification":"2025-04-18T16:28:19.818Z","creation":"2019-03-27T00:22:43Z"},"accession":"S-EPMC2689902","cross_references":{"pubmed":["19470687"],"doi":["10.1681/asn.2008040433","10.1681/ASN.2008040433"]}}