From Our 2012 Archives
Genes May Give Clues to Severe Form of Lupus
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WEDNESDAY, Jan. 18 (HealthDay News) -- Researchers have identified a DNA sequence that appears to speed up the progression of lupus, an autoimmune disease in which the body's immune system attacks healthy tissues.
"Enhancers" are DNA sequences that accelerate the activation of neighboring genes, according to Italian researchers. In the case of lupus, researchers identified a particular DNA sequence, called HS1.2, which may play a role in the most severe cases of the disease, which can cause joint pain, fever, skin rashes, hair loss and anemia.
The study's authors explained that HS1.2 leads to increased activation of the "transcription factor NF-KB" (a molecule that "reads" the genes to make them work). As a result, this accelerator boosts the production of antibodies that attack the tissues, and increases the aggressiveness of the disease.
The discovery of the accelerator could lead to more effective treatments for lupus, such as medications that "turn off" the accelerator, the study authors said.
The study appears in the Annals of the Rheumatic Diseases.
"Our results suggest that new drugs that turn off the enhancer HS1.2, or inhibit its effect on NF-KB, can stop the disease without the need for immunosuppressive drugs or other therapies with many side effects," the study's leader, Gianfranco Ferraccioli of the Catholic University of Sacred Heart in Rome, said in a university news release. "Moreover, the discovery of the role of this enhancer allows us to better classify patients and formulate a precise prognosis for each one moving toward more personalized care."
Treatments for lupus include cortisone, antimalarial drugs, immunosuppressants and biologic drugs.
HS1.2 also plays a role in other autoimmune diseases such as rheumatoid arthritis, and may increase susceptibility to autoimmune diseases, according to the news release.
-- Mary Elizabeth Dallas
Copyright © 2012 HealthDay. All rights reserved.
SOURCE: Catholic University of Sacred Heart, news release, Jan. 16, 2012
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