Study
Suggests Carbohydrates Are Attacked in Arthritis
By
KENNETH CHANG
The NY TIMES,
August 22, 2002
Scientists may have discovered an
important, unexpected clue in the long, elusive search for the cause of
rheumatoid arthritis.
Rheumatoid arthritis, a disease
without cure that afflicts more than two million people in the United
States, is thought to be caused by out-of-control immune cells that
mistakenly attack cartilage and joints.
But scientists have been unsure
exactly what in the cartilage and joints the immune cells are attacking.
In such autoimmune diseases, the
body's defense system typically turns against itself by homing in on and
destroying one of the body's proteins. Some scientists have proposed that
rheumatoid arthritis attacks collagen, a fibrous protein in cartilage,
bone and connective tissues, but the evidence has been ambiguous.
The new research suggests that the
target of destruction is not a protein, but carbohydrates.
"There has to be some sort of
attraction," said Dr. Julia Y. Wang, a professor of medicine at
Harvard Medical School and Brigham and Women's Hospital in Boston.
"Our study for the first time identifies a direct link between
carbohydrates in our tissues, the immune system and rheumatoid
arthritis."
Dr. Wang and Dr. Michael H. Roehrl of
Harvard believe the target is a type of carbohydrate known as
glycosaminoglycans, a major component of cartilage, joint fluids,
connective tissue and skin.
If true, the findings could lead to
drugs that reduce or disarm the rampaging cells.
Dr. Wang presented the findings
yesterday at the national meeting of the American Chemical Society in
Boston. Other scientists will have to repeat the experiments before the
theory gains acceptance.
"I think this is of considerable
interest and potentially very important," said Dr. John H. Klippel,
medical director of the Arthritis Foundation. "It opens a new way of
thinking about this disease. We don't think of the immune system as
responding to complex carbohydrates."
In the experiments, Dr. Wang and Dr.
Roehrl injected glycosaminoglycans into mice, inducing arthritis-like
swelling and inflammation around the animals' joints. "The bones
start to erode," Dr. Wang said.
The mice also developed lesions in
their tendons and skin, also symptoms of rheumatoid arthritis.
The researchers developed a test to
find immune cells that bind to glycosaminoglycans. The test revealed high
concentrations of the cells not only in and around the mice's rheumatoid
lesions, but also in bone marrow.
Dr. Wang said she believed that the
body produces the carbohydrate-binding cells in bone marrow as a normal
matter of course to control the level of glycosaminoglycans in the blood.
When the level of the carbohydrate soars for some reason, she said, the
immune system appears to respond by churning out more immune cells and
some of the excess miss their intended targets in the blood and bind to
glycosaminoglycans in the joints instead, to disastrous effect.
Tests on joint tissue from nine human
arthritis patients showed the immune cells in people suffering from
rheumatoid arthritis, but not other forms of arthritis, which are not
autoimmune diseases. Dr. Wang said she did not know why the carbohydrate
levels might become elevated.
Rheumatoid arthritis accounts for
about 2.1 million of the 42 million cases of arthritis in the United
States and strikes fairly young in life, usually middle age, but sometimes
as early as the 20's and 30's. About three-quarters of patients are women.
Currently, some drugs alleviate the disease's painful swelling, but there
is no cure.
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