NEW YORK (Reuters Health) -- Researchers at the University of
California, San Francisco believe they have found an important new clue
to the development of multiple sclerosis (MS), which could lead to new
ways to treat the disease.
Dr. Claude Genain, a neurologist, and colleagues at UCSF and Albert
Einstein College of Medicine in New York City have discovered that
antibodies produced by B cells -- a type of white blood cell -- attack
myelin in the fatty sheath that surrounds nerves. Destruction of myelin
is a hallmark of MS, a chronic, often disabling disease of the central
nervous system that affects about 300,000 people in the US.
It has been generally accepted that development of MS is related to an
abnormal immune response directed against the central nervous system,
and over the past decade, researchers have concentrated their attention
on the role of the immune system's T cells. But the new study, published
in the journal Nature Medicine, suggests that antibodies produced by B
cells also play an important role.
Genain and his colleagues studied brain tissue taken from MS patients
and from animals with a similar disease, and were able to determine that
myelin destruction occurred only in the presence of both T cells primed
to attack myelin proteins and antibodies directed against a protein in
the protective sheath.
"I am convinced that antibodies are a major, major mechanism by which
myelin damage is produced," Genain told Reuters Health. "The clinical
implications are that we may be able to design drugs to inhibit these
antibodies, to neutralize them and arrest the progression of the
disease."
He acknowledged, however, that not all people have the same type of MS.
"We have looked at what can be called 'hot' lesions where there is
intense destructive activity, and found that these are invariably
associated with antibody deposition," he explained. "However, the
respective part played by T and B cell-mediated mechanisms may well
differ in individual cases."
Nevertheless, Genain is optimistic that drugs could be available within
several years to counter the effects of the destructive antibodies.
SOURCE: Nature Medicine February 1999.
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