New insight into the cause of multiple sclerosis
Nancy D. Lamontagne
In multiple sclerosis, inflammation
in the central nervous system leads to unsheathing of the protective myelin that
coats neurons, causing them to degenerate. Scientists have thought that the inflammation
is caused by an immune response directed against the myelin. New research lends
credence to this belief by revealing certain specifics of how the immune response
occurs. The work could help direct future research into therapies for the disease.
New research has demonstrated that an immune response against
myelin oligodendrocyte glycoprotein is involved in multiple sclerosis. These cultured
cells show a control group (top left) and cells expressing the protein (green) at
200x magnification (top right) and at 600x magnification (bottom). Images reprinted
with permission of PNAS.
Researchers at Heinrich Heine University in Düsseldorf,
Philipps University in Marburg and Georg August University in Göttingen, all
in Germany, studied the role of antibodies that attack myelin oligodendrocyte glycoprotein,
which is embedded in the myelin sheath. Their experiments revealed that these antibodies
were circulating in some patients suffering from multiple sclerosis, and they found
that cultured cells with the protein on their surface died when exposed to the antibodies.
Studies using rats showed that demyelination and neuronal damage occurred in animals
exposed to antibodies against the glycoprotein. The work is detailed in a soon-to-be-published
PNAS paper (doi/10.1073/pnas.0607242103).
In their studies with rats, researchers found that human antibodies
directed against myelin oligodendrocyte glycoprotein bind to intact myelin. The
left images show rat brain slices that were positive for antibodies against the
glycoprotein (shown as green), and the right image shows a slice that was negative
for the antibodies.
From these findings, the researchers
concluded that, in a subgroup of multiple sclerosis patients, antibodies directed
against myelin oligodendrocyte glycoprotein caused the neuron damage. Future research
will be needed to determine how this immune response relates to clinical and pathological
characteristics of the disease and whether an immune response to other proteins
also plays a role.
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