期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 35, 期 4, 页码 1143-1154出版社
WILEY
DOI: 10.1002/eji.200425861
关键词
NKT cells; CD1d; systemic lupus erythematosus; glycolipids; immunotherapy
类别
资金
- NHLBI NIH HHS [P01 HL068744, HL68744] Funding Source: Medline
- NIAID NIH HHS [R01 AI042284, R01 AI050953, AI42284, AI50953, R01 AI043407-09, R01 AI043407, AI43407, R21 AI042284] Funding Source: Medline
- NIAMS NIH HHS [R01 AR047322-04, R01 AR047322, AR47322] Funding Source: Medline
- NINDS NIH HHS [R01 NS044044, NS44044] Funding Source: Medline
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 alpha-galactosylceramide (a-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 a-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 a-GalCer suppresses or promotes pristane-induced lupus-like autoimmunity in mice, in a strain-dependent manner.
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