Abstract
Systemic lupus erythematosus is a systemic autoimmune disease characterized by inflammation in organs such as kidneys and presence of autoantibodies against nuclear antigens. We have previously shown that CD1d deficiency in BALB/C mice exacerbates lupus nephritis and autoantibody production induced by the hydrocarbon oil pristane. Here, we have tested the impact of activating CD1d-restricted natural killer T (NKT) cells on pristane-induced lupus-like autoimmunity in BALB/c and SJL mice. Repeated in vivo treatment of pristane-injected BALB/c mice with the NKT cell ligand α-galactosylceramide (α-GalCer) prior to the onset of florid disease suppressed proteinuria, in a manner that was dependent on CD1d and IL-4 expression. In sharp contrast, however, similar treatment of pristane-injected SJL mice with α-GalCer resulted in increased proteinuria. Consistent with these dichotomous effects of NKT cell activation on the development of lupus-like autoimmunity, NKT cells in BALB/c and SJL/J mice exhibited a mixed Th1 /Th2 and a Th1-biased cytokine production profile, respectively. These findings demonstrate that NKT cell activation with α-GalCer suppresses or promotes pristane-induced lupus-like autoimmunity in mice, in a strain-dependent manner.
Original language | English (US) |
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Pages (from-to) | 1143-1154 |
Number of pages | 12 |
Journal | European Journal of Immunology |
Volume | 35 |
Issue number | 4 |
DOIs | |
State | Published - Apr 2005 |
Keywords
- CD1d
- Glycolipids
- Immunotherapy
- NKT cells
- Systemic lupus erythematosus
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology