Scientists Find New Key to Lupus

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Scientists Find New Key to Lupus

Molecule identified in lab mice may cause autoimmune disease

October 19, 2009
 
 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.

SOURCE: US NEWS & WORLD REPORT

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STANFORD, Calif., Oct. 21 (UPI) -- U.S. medical investigators say they have identified in mice a pathway that causes a lupus-like autoimmune disease.

Stanford University scientists say their discovery involves macrophages -- part of the body's immune system that are responsible for disposing of dying cells.

The study showed if the disposal process is disrupted, the lupus-like disease develops.

Researcher Lata Mukundam, one of the authors of the study, said that finding could lead to both a better understanding of the cause of lupus in humans and potential drug treatments for the disorder.

"Just like in mice, … if you don't clear the dying cells, then that predisposes you to lupus," Mukundan said. "If you look at patients with lupus, they have an inability to clear those dead cells."

Assistant Professor Ajay Chawla, senior author of the study, added: "The clearing away of dying cells is important. If they're not cleared away, they can provide antigens against ourselves, leading to development of autoimmunity."

Lupus is an autoimmune disease in which the body attacks its own cells. The chronic inflammation causes symptoms that can resemble other types of arthritis and rheumatic diseases, affecting the skin, heart, lungs, kidneys, joints and nervous system, researchers said. The cause is unknown.

The study appears in the early online edition of the journal Nature Medicine.