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Article Dans Une Revue Journal of the American Society of Nephrology Année : 2009

Invariant natural killer T cells and TGF-ß attenuate anti-GBM glomerulonephritis

Résumé

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 (J alpha 18(-/-)) 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 J alpha 18(-/-) mice. Interestingly, expression of both TGF-beta and TGF-beta-induced (TGFBI) mRNA was higher in wild-type kidneys compared with J alpha 18(-/-) 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 J alpha 18(-/-), mice. In conclusion, in experimental anti-GBM GN, iNKT cells attenuate disease severity and TGF-beta has a renoprotective role.
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Dates et versions

hal-02658566 , version 1 (30-05-2020)

Identifiants

Citer

L. Mesnard, A.D.C. Keller, M.L. Michel, S. Vandermeersch, C. Rafat, et al.. Invariant natural killer T cells and TGF-ß attenuate anti-GBM glomerulonephritis. Journal of the American Society of Nephrology, 2009, 20 (6), pp.1282-1292. ⟨10.1681/ASN.2008040433⟩. ⟨hal-02658566⟩
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