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.
And researchers at the Stanford University School of Medicine now think antibodies' absence in the central nervous system (the brain and spinal cord) may be a key part of the reason why nerve damage there doesn't get naturally repaired in humans.
That insight could someday lead to new treatments for stroke and spinal-cord trauma.
In a new study conducted in mice, to be published online June 14 in Proceedings of the National Academy of Sciences, the Stanford scientists show for the first time that antibodies are critical to the repair of nerve 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 those proteins' unanticipated nurturing qualities may lead to new ways of repairing damage from stroke or spinal-cord injury, as well.
"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," said senior study author Ben Barres, MD, PhD, professor and chair of neurobiology. So his group was intrigued by one major difference between the two nervous systems: Antibodies, which are large bulky proteins, 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.
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