OT: Antibodies help repair nerve cells; except in the spine and brain.

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Antibody surprise

Antibodies — warrior proteins the immune system makes to defend the body against

invading pathogens such as viruses and bacteria — have a gentler side nobody

knew about until now: They function not only as soldiers but also as nurses.

" In an injured human brain or spinal cord, the degenerating myelin just sits

there for the rest of the person's lifetime. But after injury to, say, the

sciatic nerve, the degenerating myelin is cleared within a week or less. "

And researchers at the School of Medicine now think antibodies' absence in the

central nervous system (the brain and spinal cord) might be a key reason nerve

damage there doesn't get naturally repaired in humans.

In a study conducted in mice, published online June 14 in Proceedings of the

National Academy of Sciences, the Stanford scientists showed for the first time

that antibodies are critical in repairing damage to the peripheral nervous

system — nervous tissue that extends outside the brain and spinal cord, such as

the sciatic nerve, where circulating antibodies have access. The study also

shows that some, but not all, antibodies get the job done. Harnessing the

unanticipated nurturing qualities of these proteins might lead to new ways of

repairing damage from stroke or spinal-cord injury.

" Nobody has known why, but nerve cells in the central nervous system fail to

regenerate after injury whereas those in the peripheral nervous system

regenerate robustly, " says senior study author Ben Barres, MD, PhD, professor

and chair of neurobiology.

His group was intrigued by one major difference between the two nervous systems:

Antibodies have limited access to the brain and spinal cord (these organs are

surrounded by an interface called the blood-brain barrier or, in the spinal

cord, the blood-spinal cord barrier), while they have ready access to the

peripheral nervous system.

Nerve cells convey electrochemical impulses over long distances by means of

long, tubular projections called axons. These axons are typically wrapped in an

insulating layer of a fatty substance called myelin.

" After nerve injury, the degenerating myelin downstream from the injury is

rapidly cleared in the peripheral, but not the central, nervous system, " says

Barres. " In an injured human brain or spinal cord, the degenerating myelin just

sits there for the rest of the person's lifetime. But after injury to, say, the

sciatic nerve, the degenerating myelin is cleared within a week or less. "

The researchers wondered whether antibodies might play a role in that clearance.

They obtained mutant laboratory mice that can't make antibodies, and

demonstrated that repair of injury to the sciatic nerve is substantially

impeded, as is the removal of degenerating myelin downstream from the injury

site. Simply injecting the injured mutant mice with antibodies from healthy,

uninjured ones restored both myelin removal and sciatic-nerve repair capability

in the mice.

While antibodies have been found to play a role in the disposal of aging red

blood cells, this is the first time they've been implicated in injury repair,

say the researchers. What's more, they threw light on the way in which this

happens: Antibodies grab onto the degenerating myelin downstream from the site

of the nerve injury, tagging the myelin for clearance by immune cells called

macrophages. — Bruce Goldman

http://stanmed.stanford.edu/2010fall/upfront.html#c