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Development of a systemic autoimmune disease
Development of a systemic autoimmune disease -- Posted by doe on 06-03-04 16:43
Seems like a lack of antioxidants to decrease the oxidation / rust .. leads to
.. autoimmune disease ...
<>
These data strongly suggest that a deficiency in detoxification and increased
oxidative stress can result in the development of a systemic autoimmune
disease.
<>
Physiol Genomics. 2004 Jun 1 [Epub ahead of print] Related Articles, Links
Genetic Dissection of Systemic Autoimmune Disease in Nrf2 Deficient Mice.
Li J, Stein TD, Johnson JA.
School of Pharmacy, University of Wisconsin, Madison, WI, USA.
Systemic lupus erythematosus (SLE) is an autoimmune disorder with
immune-complex deposition that affects multiple organs. Previous studies have
suggested the involvement of oxidative stress and apoptosis in SLE, but no
clear link to etiology has been established. Here we show that mice deficient
in a transcription factor responsible for controlling the expression of
numerous detoxification and antioxidant genes develop an autoimmune disease
with multiple organ pathologies that closely resembles human SLE. Aged female
mice with a knockout of nuclear factor, erythroid derived 2, like 2 (nrf2) are
prone to develop antibodies against double stranded DNA and the Smith antigen
as well as IgG, IgM, and C3 deposition in kidney, liver, heart, and brain.
Prior to the development of autoimmune antibodies and organ pathology,
oxidative damage occurs in the liver and kidney as indicated by the increased
levels of the DNA oxidation marker 8-hydroxydeoxyguanosine and the later
increase in the lipid peroxidation product malondialdehyde. Gene expression
profiles demonstrate an early decrease in numerous antioxidant and
detoxification genes in the livers and altered levels of cytokines and T and B
cell-specific genes in the spleens of nrf2 knockout mice. These data strongly
suggest that a deficiency in detoxification and increased oxidative stress can
result in the development of a systemic autoimmune disease.
PMID: 15173550 [PubMed - as supplied by publisher]
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