It is already known that Natural Killer cells play an important role in fighting cancer, in both mice and humans. In some cancer treatments, their function is enhanced by using drugs to make the cells more active.
In this new pain research, funded by the National Research Council of Korea, the MRC, NIH and ERC, the team used a similar approach to make the Natural Killer cells more effective in removing damaged nerve fibres in mice. They showed that better removal of these damaged fibres reduced the hypersensitivity associated with chronic nerve pain.
Alexander Davies of Oxford’s Nuffield Department of Clinical Neurosciences said: ‘Long-term pain from nerve injury remains a challenge for modern medicine because we have no way of removing damaged nerve fibres without causing more injury.
‘Our research shows that the immune system is actually capable of removing these damaged axons to allow for the re-growth of healthy ones.
‘If we can tailor current treatments to help the Natural Killer cells remove damaged nerves we may have a way to speed the recovery from a painful nerve injury without the narcotic side-effects of other pain killers.
‘Our next goal is of course to translate these findings from mice into people.’
The scientists are now keen to verify whether the same naturally occurring mechanism that they have discovered in mice is also at play in the damaged nerves of humans.
As to why some people get better after nerve injury, while others don’t heal so well or so quickly, this may be explained by differences in how effective an individual’s immune system is at clearing away damaged nerve fibres.
Treatments that enhance the function of the Natural Killer cells could help remove the ‘faulty wiring’ of damaged nerves. This approach could be of much more long-term benefit for patients with chronic pain than the use of opioids, which temporarily silence the nerves, but do not fix the underlying damage causing the pain.
The full paper, ‘Natural Killer Cells Degenerate Intact Sensory Afferents Following Nerve Injury,’ can be read in Cell Press.