As we age our stem cells lose their ability to field new immune cells, but deleting the Per2 gene in mice can boost the ailing immune system and even extend lifespan in mice
The elderly are far more vulnerable to new diseases and infection than the young, and one of the reasons for that is that hematopoietic stem cell (HSC) function declines – producing a dwindling supply of new immune soldiers. The body retains many old veteran cells that protect you from disease you’ve developed immunity to, but when it comes to new pathogens we need a fresh supply of healthy cells. This supply is compromised as you get older. While there are other reasons for immune decline like the shrinking thymus, there is evidence that accumulated DNA damage to these HSCs impairs function.
Switching off Per2
Per2 is involved in circadian rhythm regulation, which is essentially your sleep/wake cycle. The researchers found that this Per2 gene limited HSC self renewal following DNA damage, which meant less stem cells were available to form new immune cells. When they deleted it in mice, this appeared to stabilise the population and maintained production of new lymphocytes. Once more, it even extended the lifespan of these mice by up to 15% – highlighting how important a healthy immune system is.
This deletion surprisingly helps aging, flagging immune systems by limiting the effect of age on HSCs. While the deletion in itself doesn’t correct the issue at hand, DNA damage, it does prevent HSCs from diminishing by limiting their ability to sense this damage. While this might seem like a protective response to aging damage, many processes in the aging body appear to actually make things worse; supporting the evolutionary theory of aging. In the future we’ll need to either replenish damaged HSCs with new cells, or find a way to correct DNA damage, in order to fully correct the problem.
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