Protein May Be Key to Rheumatoid Arthritis

Finding could lead to new therapies for the disease, study suggests.

By Janice Billingsley
HealthDay Reporter
Thursday, March 29, 2007; 12:00 AM

Copyright © 2007 ScoutNews, LLC. All rights reserved.

WEDNESDAY, March 28 (HealthDay News) -- In the quest for the causes of and potential treatments for rheumatoid arthritis, Japanese researchers have identified a protein that could be a target for future therapy.

Rheumatoid arthritis (RA) is a chronic and disabling autoimmune disease that first attacks the fluid that surrounds the joints, causing it to thicken and grow abnormally, damaging the joints and surrounding cartilage rather than protecting them. More than 2 million Americans suffer from the illness, according to the Arthritis Foundation.

By identifying a protein that appears to be one of the culprits in the unhealthy buildup of this fluid, which is called synovial fluid, Dr. Yasushi Miura and his colleagues at Kobe University School of Medicine hope that a new, targeted medication can be developed to treat the disease.

"The protein Decoy receptor 3 (DcR3) is one of the pathological factors of RA and can be a new therapeutic target for treatment," said Miura, an associate professor in the division of orthopedic sciences at the medical school.

His findings are published in the April issue of Arthritis & Rheumatism, the journal of the American College of Rheumatology.

DcR3 is a member of the large tumor necrosis factor receptor (TNFR) "super family," which has been identified in the last decade as important in the regulation of cell growth and cell death, fundamental processes in biology, said Dr. Robert Hoffman, director of the division of rheumatology and immunology at the University of Miami Miller School of Medicine in Florida.

"We have known of the importance of cell growth and cell death in studying cancer but more recently have found that it is also important in autoimmune diseases like RA and lupus," he said.

It was the similarity between the growth of malignant tumors and the abnormal growth of synovial tissue, called hyperplasia, that sparked Miura's research into DcR3 and rheumatoid arthritis. DcR3 is known to be produced in tumor cells, including lung and colon cancers.