Researchers outline Lupus gene ending
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 of 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. Klippel, medical director for the Arthritis Foundation and formally a Lupus expert at the National Institutes of Health. “It should not take them very much time at all to move into human genetic research”.
Lupus is an autoimmune disease, meaning the body’s own defenses attack its health 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 have a ripple effect.”