Samuel Strober

Publication Details

  • beta-galactosylceramide alters invariant natural killer T cell function and is effective treatment for lupus CLINICAL IMMUNOLOGY Morshed, S. R., Takahashi, T., Savage, P. B., Kambham, N., Strober, S. 2009; 132 (3): 321-333

    Abstract:

    NZB/W female mice spontaneously develop systemic lupus, an autoantibody mediated disease associated with immune complex glomerulonephritis. Natural killer (NK) T cells augment anti-dsDNA antibody secretion by NZB/W B cells in vitro, and blocking NKT cell activation in vivo with anti-CD1 mAb ameliorates lupus disease activity. In the current study, we show that beta-galactosylceramide reduces the in vivo induction of serum IFN-gamma and/or IL-4 by the potent NKT cell agonist alpha-galactosylceramide and reduces NKT cell helper activity for IgG secretion. Treatment of NZB/W mice with the beta-galactosylceramide ameliorated lupus disease activity as judged by improvement in proteinuria, renal histopathology, IgG anti-dsDNA antibody formation, and survival. In conclusion, beta-galactosylceramide, a glycolipid that reduces the cytokine secretion induced by a potent NKT cell agonist ameliorates lupus in NZB/W mice.

    View details for DOI 10.1016/j.clim.2009.05.018

    View details for Web of Science ID 000268783900004

    View details for PubMedID 19564135

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