British scientists have made a double breakthrough which could help reverse some of the effects of ageing, it was announced last night.
The researchers in Edinburgh have successfully persuaded the thymus, a key part of the immune system, to regenerate itself.
Their experiment was performed on elderly mice.
The researchers say it is the first time the science of regenerative medicine has been used to restore an organ in a living creature.
Their treatment led to the function of the thymus being restored in the animals and the production of more white blood cells – the T cells.
Reporting in the journal Development, the researchers say it has been achieved by targeting a single protein to reactivate a mechanism shut down by age.
The protein FOXN1 helps control genes in the thymus.
The scientists say they have yet to show that the treatment improved the strength of the animals’ immune system. As the treatment involved the use of genetically modified animals, there are also further steps to take before it can be tested in humans.
Researcher Professor Clare Blackburn, from the Medical Research Council Centre for Regenerative Medicine at Edinburgh University, said: "By targeting a single protein, we have been able to almost completely reverse age-related shrinking of the thymus.
"Our results suggest that targeting the same pathway in humans may improve thymus function and therefore boost immunity in elderly patients, or those with a suppressed immune system. However, before we test this in humans we need to carry out more work to make sure the process can be tightly controlled."
Dr Rob Buckle, the MRC’s head of regenerative medicine, said: "Previous attempts to provoke thymus regeneration have involved using sex hormones, but these have resulted in only temporary recovery of size and function of the organ.
"In this study, the recovery of the thymus was sustainable, but more work is needed to ensure there are no unintended consequences of increasing FOXN1."
Bredenkamp et al. Regeneration of the aged thymus by a single transcription factor. Development 8 April 2014; doi:10.1242/dev.103614

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