Arthritis Under Assault
Posted on: Thursday, 7 February 2008, 21:00 CST
By Abram Katz
Register Science Editor Many people think of arthritis as minor aches and pains. For most people, that's all it is.
But, about 1 percent of the adult population -- some 2.1 million people, two-thirds of them women -- have rheumatoid arthritis, which is far more than wear and tear of the joints.
Rheumatoid arthritis is believed to be an autoimmune disease, which means the sufferer's own immune system mistakenly attacks tissue that surrounds the joints. The complex disease probably is influenced by genetic and environmental factors, too.
The American College of Rheumatology has launched a campaign to investigate the causes of the disease and researchers at the Yale School of Medicine have received one of the organization's initial research grant.
Yale immunobiologists plan to use the $200,000 to explore the role of certain elements of the immune system, called interleukins, in the development and progress of the debilitating condition.
"Treatments have improved, but there is no cure and we have a long way to go," said Dr. James O'Dell, president of research and education at the American College of Rheumatology.
O'Dell said the collective research effort is informally called the "within our reach" campaign "because we're close. We know more about genetics and the immune system."
Eventually, it may be possible to identify people likely to develop the disease and begin treatment before symptoms occur, O'Dell said.
About one year ago, the college of rheumatology interviewed rheumatoid arthritis experts and decided to award research grants, he said.
Research on the disease is "relatively underfunded," O'Dell said.
"Our goal is to raise $30 million over the next five years. The donation focus is on families with members who have rheumatoid arthritis. We currently have about $8 million. The first round of grants was awarded to 15 recipients," he said.
Rheumatoid arthritis is an inflammatory disease that causes pain and difficulty of movement, according to the American Arthritis Foundation. Unlike "wear and tear" osteoarthritis, rheumatoid arthritis is generally symmetrical, meaning that both knees, hands or wrists are affected.
People with the disease may also develop anemia and other problems, such as fatigue, neck pain, and dry eyes and mouth. Blood vessels may be damaged.
In normal joints, bones capped with cartilage meet in a capsule containing synovial fluid, which lubricates and nourishes the joints. A layer of tissue in the joint, called the synovium, produces this fluid.
In rheumatoid arthritis, the synovium becomes inflamed and swollen, O'Dell said. As the disease progresses, the synovium spreads throughout the joint, covering tendons, ligaments and muscles. The weakened joint structure may then twist out of shape.
"There is a powerful genetic component. At least five or six genes are important. The are also environmental factors," O'Dell said.
"We know that there are genes that increase the risk of rheumatoid arthritis and other autoimmune diseases, such as lupus," he said.
At Yale, Dr. Richard A. Flavell, chairman of immunobiology, and Zhinan Yin, assistant professor of rheumatology, are using the grant to study genes as a way of examining the immune system's role in rheumatoid arthritis.
Specifically, the group is interested in interleukins, which are created by different immune system cells in response to infection.
Since this research cannot be done in people, the lab uses mice genetically engineered to have collagen arthritis, which is believed to be analogous to rheumatoid arthritis in humans.
Elizabeth Eynon, associate research scientist in immunobiology, said murine genes are altered to answer questions about the immune system, interleukins and the roots of rheumatoid arthritis.
"We want to look at how interleukin-10 (IL-10) functions in arthritis. IL-10 is anti-inflammatory, it turns off the immune system," Eynon said.
Another cytokine, interleukin-17 (IL-17), triggers inflammation. Scientists suspect that IL-10 may play a part in regulating IL-17. Perhaps rheumatoid arthritis occurs when the IL-10 system is either blocked, inhibited or somehow rendered abnormal, Eynon said.
"We're looking at a little window of the disease process, and whether we can influence the balance of IL-10 and IL-17. This is basic research on why the immune system is not regulating itself," she said.
Given the complexity of the immune system and its relationship to the environment, IL-10 and IL-17 interactions are probably part of a larger process gone awry, she said.
When the regulation of inflammation is understood, results could be applied to other autoimmune diseases, such as multiple sclerosis, scleroderma, lupus and possibly diabetes, Eynon said.
O'Dell said an initial infection may set off the immune response that leads to rheumatoid arthritis. Other environmental assaults could also play a part.
"In certain people, smoking increases the risk of rheumatoid arthritis. That's just one factor in 20 percent of the patients," he said.
While no new medicines are expected to emerge immediately from the basic research at Yale, there are about 17 drugs approved to modify the course of rheumatoid arthritis.
Nonsteroidal anti-inflammatories are widely used. Corticosteroids can be administered to relieve inflammation and swelling. Medications that reduce the strength of the immune system are also used, as are newer drugs that block specific parts of the immune system.
Abram Katz can be reached at akatz@nhregister.com or 789-5719.
(c) 2007 New Haven Register. Provided by ProQuest Information and Learning. All rights Reserved.
Source: New Haven Register
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