The link with arthritis
“We are very excited to have Diane
and Christophe join Joslin’s Research Division. The work of the Benoist/Mathis
lab is important not only for understanding diabetes, but also for other
diseases,” says George King, M.D., Acting Director of Research at Joslin. “They
will be taking the lead in the area of autoimmunity in the development of type
1 diabetes and transplant rejection, which are critical areas of development
for the control of diabetes.” Drs. Benoist and Mathis receive funding from the
Juvenile Diabetes Foundation (JDF) for their work on behalf of JDF’s Center for
Islet Transplantation at Harvard Medical School.
Coincidentally, their studies of
the body’s autoimmune response have shed light on another disease in which the
body’s immune system turns against self-tissue — rheumatoid arthritis.
Rheumatoid arthritis affects 2.1 million Americans, mostly women.
“By chance, one of the more than
100 strains of mice in which we study diabetes developed arthritis and so we
started working on it,” Dr. Mathis says.
Earlier this year, the research
team and their French colleagues published a paper in the journal Science reporting
that they had identified a particular protein that is the target of an
autoimmune response in arthritic mice. Joint destruction in rheumatoid
arthritis is believed to be caused by an immune system attack against tissue in
the joints, although prior to their findings, the antigen that causes
the response had not yet been identified. Isao Matsumoto, M.D., of Joslin, a
research fellow in the Benoist/Mathis lab, found the problem protein does not
reside specifically in the joints, as many researchers had previously thought,
but it in an enzyme (protein) called glucose-6-phosphate isomerase (GPI).
To identify the immune system
target, the researchers extracted cells from various tissue in normal and
arthritic mice. Dr. Matsumoto found that the GPI protein was associated with
antibodies in the mice with arthritis. “We then tested our theory in a number
of ways. After injecting anti-GPI antibodies in mice that did not have arthritis,
the mice did develop the disease,” Dr. Benoist says.
Why, if the target is found
throughout the body, does this destruction occur in the joints? “We suspect
that some unusual physiological feature of joints may be responsible for
focusing the autoimmune destruction in that area,” Dr. Benoist says. “It is
really a puzzle at present, but one which should bring important developments
in the future.”
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