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Nephrology Dialysis Transplantation, Vol 14, Issue 90001 14-16, Copyright © 1999 by Oxford University Press


ORIGINAL ARTICLES

T cell subsets in experimental lupus nephritis: modulation by bacterial superantigen

E De Heer, L Aaldering and S Florquin
Leiden University Medical Center, Department of Pathology, LI-Q, PO Box 95600, 2300 RC, Leiden, The Netherlands; Corresponding author

Chronic graft-vs-host disease (GvH), induced by injection of DBA/2 lymphocytes into (C57BL/6 x DBA/2)F1 hybrids, is a murine model for lupus nephritis, associated with a Th2-dependent polyclonal B cell activation. The development of glomerulosclerosis in this model is preceded by a glomerular influx of LFA-1+ T cells. We investigated whether exposure to bacterial superantigen would modulate the course of this autoimmune syndrome. Injection of the bacterial superantigen staphylococcal enterotoxin B (SEB) in mice has been shown to induce the activation of TcRV{beta}8+ T cells. Within 2 weeks after GvH induction, mice were injected twice with 20 &mgr;g of SEB and the following parameters were examined: cytokine and Ig profile, proteinuria and renal pathology. The second SEB injection induced in GvH mice an increased release of both interferon-&ggr; (IFN-&ggr;) and interleukin-10 (IL-10) as compared with control F1 mice. No differences were observed in IL-2 production. SEB-treated GvH mice demonstrated a delayed onset of proteinuria. Histological analysis of the kidney showed that SEB-challenged GvH mice displayed significantly more interstitial inflammation and mesangial proliferation together with more IgG2a deposits in glomeruli than non-injected GvH mice. From these results, we conclude that GvH mice are more responsive to SEB in terms of cytokine production and that bacterial infection can modulate the course of this renal disease from a membranous to a more proliferative type of nephropathy.Keywords: graft-vs-host disease; lupus nephritis; staphylococcal enterotoxin G; superantigen; cytokines
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