Journal
JOURNAL OF IMMUNOLOGY
Volume 171, Issue 4, Pages 2142-2153Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.171.4.2142
Keywords
-
Categories
Funding
- NHLBI NIH HHS [HL68744] Funding Source: Medline
- NIAID NIH HHS [AI44074, AI42284, AI50953] Funding Source: Medline
- NIAMS NIH HHS [AR47322, R01 AR047322-03] Funding Source: Medline
Ask authors/readers for more resources
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that is accompanied by the emergence of autoreactive T cells and a reduction in regulatory T cells. Humans and mice with SLE have reduced numbers of CD1d-restricted NK T cells, suggesting a role for these cells in the regulation of SLE. In this study, we show that CD1d deficiency exacerbates lupus nephritis induced by the hydrocarbon oil pristane. This exacerbation in disease is associated with: 1) reduced TNF-alpha and IL-4 production by T cells, especially during the disease induction phase; and 2) expansion of marginal zone B cells. Strikingly, inoculation of pristane in wild-type mice resulted in reduced numbers and/or functions of NK T cells and CD1d-expressing dendritic cells. These findings suggest that CD1d may play an immunoregulatory role in the development of lupus in the pristane-induced model.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available