Journal
IMMUNOLOGY
Volume 128, Issue 1, Pages e306-e314Publisher
WILEY-BLACKWELL PUBLISHING, INC
DOI: 10.1111/j.1365-2567.2008.02964.x
Keywords
andrographolide; autoimmunity; dendritic cells; nuclear factor-kappa B; rosiglitazone; systemic lupus erythematosus
Categories
Funding
- FONDECYT [1050979, 1070352]
- Proyecto [PBCT RED15]
- FONDEF [D04I1075]
- Millennium Nucleus on Immunology and Immunotherapy [P04/030-F]
- VRAID
- CONICYT
- [INCO-CT-2006-032296]
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P>Autoimmune diseases, such as systemic lupus erythematosus (SLE), result from deficiencies in self-antigen tolerance processes, which require regulated dendritic cell (DC) function. In this study we evaluated the phenotype of DCs during the onset of SLE in a mouse model, in which deletion of the inhibitory receptor Fc gamma RIIb leads to the production of anti-nuclear antibodies and glomerulonephritis. Splenic DCs from Fc gamma RIIb-deficient mice suffering from SLE showed increased expression of co-stimulatory molecules. Furthermore, diseased mice showed an altered function of the nuclear factor-kappa B (NF-kappa B) transcription factor, which is involved in DC maturation. Compared with healthy animals, expression of the inhibitory molecule I kappa B-alpha was significantly decreased in mice suffering from SLE. Consistently, pharmacological inhibition of NF-kappa B activity in Fc gamma RIIb-deficient mice led to reduced susceptibility to SLE and prevented symptoms, such as anti-nuclear antibodies and kidney damage. Our data suggest that the occurrence of SLE is significantly influenced by alterations of NF-kappa B function, which can be considered as a new therapeutic target for this disease.
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