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Immune
System May Trigger a
Form of Heart Disease
NEW YORK (Reuters
Health) - The chronic heart muscle disorder known as dilated cardiomyopathy
is thought to be brought on by a variety of factors--from heredity
to chronic, heavy drinking. Now, new research in mice suggests
that in some cases, the body's own immune system may be behind
the life-threatening condition.
Dilated cardiomyopathy
is marked by diseased heart muscle fibers that result in abnormal
enlargement of one or more of the heart's chambers. This weakens
the heart's ability to pump efficiently and can trigger heart
failure. Although in some cases clear genetic or environmental
causes can be determined, in other cases the cause may remain
unknown.
But one explanation
may rest in the body's immune system, according to study findings
published in the January 12th issue of Science. Japanese researchers
report that in some cases, a misguided immune system assault may
inflict the damage seen in dilated cardiomyopathy.
Dr. Tasuku
Honjo of Kyoto University in Japan led the study. Honjo told Reuters
Health that researchers have speculated the disease may involve
an abnormal immune response because some patients have been shown
to have antibodies to their own muscle protein and to certain
chemical receptors.
However, Honjo
noted, it has been unclear whether these so-called ``autoantibodies''
are the cause or a result of dilated cardiomyopathy.
In the current
study, the investigators found that a strain of mice lacking an
immune system regulator known as PD-1 developed a form of dilated
cardiomyopathy. All of the affected mice showed autoantibodies
to a protein on the surface of heart muscle cells.
Honjo's team
also found that a second strain of mice without PD-1 did not develop
the heart disease. This, they report, suggests that other genetic
factors are also involved.
If these findings
are confirmed in humans, it may be possible to treat some cases
of dilated cardiomyopathy with drugs that suppress the immune
system or possibly with gene therapy, Honjo said.
SOURCE: Science
2001;291:319-322.
Reference
Source 89
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