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News Briefs
Genetic Signature Linked to Severe Lupus Symptoms
Scientists have discovered a genetic signature present in some patients with
systemic lupus erythematosus (SLE) that may help identify those at greater risk
for developing severe complications including blood disorders, central nervous
system damage, and kidney failure. Lupus is a chronic, inflammatory, autoimmune
disease. Its symptoms range from unexplained fever, swollen joints, and skin
rashes to severe organ damage of the kidneys, lungs, or central nervous system.
It affects women nine times more often than men. The current research may also
have implications for other autoimmune and inflammatory disorders.
Using DNA microarrays - small silicon chips that contain tiny amounts of thousands
of known genes - to carry out a technique called gene expression profiling,
the researchers analyzed thousands of genes in the peripheral blood cells of
48 lupus patients and 42 healthy people. Of the genes studied, 14 were linked
to a subset of SLE patients with severe disease. In addition, 161 of the genes
studied showed different expression patterns in SLE patients than in people
without lupus.
The 14 genes, referred to collectively as the IFN (interferon) expression signature,
are turned on by the activity of interferon, a complex family of proteins involved
in the regulation of immune responses. "Patients with severe SLE consistently
showed higher expression levels of this IFN signature," said Timothy W.
Behrens, MD, of the University of Minnesota, the principal investigator. Dr.
Behrens and colleagues from North Shore Long Island Jewish Research Institute
believe the data provide strong support for developing new therapies to block
IFN pathways in patients with severe lupus.
The research was featured in the online edition of the Proceedings of the National
Academy of Sciences during the week of February 10, 2003. Primary funding is
provided by the National Institute of Arthritis and Musculoskeletal and Skin
Diseases (NIAMS) of the National Institutes of Health (NIH).
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