Molecule identified in lab mice may cause autoimmune disease
MONDAY, Oct. 19 (HealthDay News) -- Researchers say they've gained new understanding of how lupus develops in mice, a finding that could help future treatments for the autoimmune disease.
An estimated 1.5 million to 2 million people in the United States suffer from lupus, a disorder in which the body's defenses turn inward. The condition can cause symptoms similar to those of arthritis and rheumatic diseases.
At issue is the immune system's ability to take out the trash -- to get rid of cells that don't have long to live. "Just like in mice, in humans, if you don't clear the dying cells, then that predisposes you to lupus," said Lata Mukundan, a Stanford University School of Medicine researcher and co-author of a study published online Oct. 18 in the journal Nature Medicine.
"If you look at patients with lupus, they have an inability to clear those dead cells," Mukundan said in a statement.
The study authors report that they gained insight into how immune-system cells detect which other cells are dying in order to dispose of them. They looked at human and mouse cells outside the body and in genetically engineered mice.
The researchers suspected that a molecule known as PPAR-delta was crucial to the process. "We wanted to know, if you took a mouse and only deleted PPAR-delta from its macrophages, is that sufficient to cause an autoimmune disease?" asked Dr. Ajay Chawla, assistant professor of endocrinology and co-author of the study, in a statement. "Apparently it is," he said.
The researchers say currently existing drugs activate the molecule in question. Perhaps, they say, the drugs could treat lupus.
Learn more about lupus from the National Institutes of Health.
SOURCE: Stanford University, news release, Oct. 18, 2009
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