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Colorado researchers working with bioengineered mice
say they have identified the first gene that increases the risk
of developing lupus, a crippling and sometimes fatal inflammatory
disease.
The researchers said that while problems with gene
Ifi202 are specifically associated with lupus, many other subtle
gene abnormalities are believed to be involved in the complex disorder.
The research, published in the September issue of
the journal Immunity, is confined to mice bred to be susceptible
to the disease. The finding still needs to be duplicated by other
labs and new studies must be conducted to see if the gene is found
in humans with lupus.
``We believe this is one piece of the puzzle,'' said
the study's senior investigator, Brian Kotzin of the University
of Colorado Health Sciences Center in Denver.
Other researchers said the gene's discovery, if confirmed,
would be ``very, very exciting.''
``If it turns out to be true, it would be an enormous
advance,'' said Dr. John Klippel, medical director for the Arthritis
Foundation and formerly a lupus expert at the National Institutes
of Health (news - web sites). ``It should not take them very much
time at all to move into human genetic research.''
Lupus is an autoimmmune disease, meaning the body's
own defenses attack its healthy tissues. Many people with lupus
also develop arthritis. In serious cases, it can attack the DNA
and proteins in the healthy cells of kidneys and other vital organs.
It mostly strikes women of childbearing age. Genetic
factors are believed to predispose some people to lupus, although
environmental factors such as infection, drug reactions, hormones
and stress may trigger it. Steroids and chemotherapy are used to
treat its symptoms, but there is no cure.
Researchers have been searching for a lupus gene for
several years. In 1997, a UCLA group retracted a study claiming
to identify a lupus gene when other labs could not duplicate the
work.
A research team at the University of Texas Southwestern
Medical Center in Dallas is investigating a cluster of different
genes that, depending on their interaction, may trigger lupus or
suppress it.
Last year, German researchers reported that the failure
of a key enzyme to mop up dying cells also contributes to lupus.
Lupus appears to share many similarities with diabetes,
rheumatoid arthritis and other autoimmune diseases, and Kotzin's
research may have broader impacts.
``All autoimmune diseases are in some way related,''
Klippel said. ``This advance could have a ripple effect.''
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