Magazine article Science News

Mouse Tests Hint at Protein's Role in Lupus

Magazine article Science News

Mouse Tests Hint at Protein's Role in Lupus

Article excerpt

Complement proteins are aptly named. These molecules help antibodies round up foreign invaders in the body and assist immune cells in removing dead cells. Like so many things, however, complement isn't fully appreciated unless it's missing.

About 90 percent of people who lack the complement protein C1q, for example, have systemic lupus erythematosus, an autoimmune disease. In such diseases, the patient's immune system attacks normal tissue.

The causes of lupus remain unclear--some patients don't lack C1q, for instance--but researchers are now shedding some light on the connection between lupus and C1q deficiency.

They have found in experiments on mice that immune systems lacking the C1q protein failed to clear away cells undergoing apoptosis, or programmed cell death, says Mark J. Walport of the Imperial College School of Medicine in London. He and his colleagues report their findings in the May Nature Genetics.

Apoptosis weeds out badly functioning or mutated cells.

Normally, complement helps immune cells called macrophages remove such dying cells. Macrophages "move in and sweep up" before the rest of the immune system can recognize the dying cells as foreigners and mount an immune response, says John D. Mountz of the University of Alabama at Birmingham.

What happens next is mysterious, says immunologist Michael C. Carroll of Harvard Medical School in Boston. "Apoptotic cells just sort of disappear." Neighboring cells probably absorb the components of the dying cells, he suggests.

However, if apoptosis is slowed and the dying cells linger--as seems to be the case when c1q is missing--the ordeal stimulates the immune system to produce more antibodies. In lupus patients, these autoimmune reactions can cause kidney damage, skin problems, central nervous system disorders, and other symptoms. …

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