Researchers led by a team from Ben-Gurion University of the Negev in Israel have just discovered a way to destroy harmful 'senescent' cells that accumulate with age and ramp up the kind of tissue damage and inflammation that slowly brings life to a grinding halt.
The team found that CD4 T immune cells transform into assassins of the damaging tissues when biological aging is detected in the body.
The new fighters, called CD4-Eomes (after the protein they produce), have been spotted before. However, this latest study highlights for the first time how closely they're linked to senescent cells and aging at the molecular level.
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"Our findings demonstrate the fundamental role of CD4-Eomes cells in modulating tissue senescence, with implications for age-related diseases and longevity," write the researchers in their published paper.
Affectionately referred to as zombie cells, senescent tissues no longer divide into fresh new generations of cells, yet remain functional enough to churn out molecules that trigger inflammation in their local environment.
Specialized units that attack senescent cells tend to be more abundant as we approach old age, previous studies have shown, prompting researchers to take a closer look at the CD4-Eomes cells to see precisely what they were doing.
By comparing the cells in mice at different ages, the researchers made two key findings.
First, the switch to CD4-Eomes was triggered by the presence of senescent cells, as if the immune system detects the risk of pending inflammation and adapts accordingly.
Second, when the mice were genetically edited to remove CD4-Eomes specializations, senescent cells became even more abundant. It's direct evidence that CD4-Eomes immune cells are keeping senescent cells in check.
Further experiments showed similar protective effects in chronic disease, specifically in a mouse model of liver cirrhosis. Scarring was reduced and senescent cell levels dropped when the CD4-Eomes cells were present.
The study demonstrates how immune systems can adapt to combat aging over time, and that there are elements of an older immune system (specifically CD4-Eomes cells) that need to be considered in anti-aging research.
"People say that to reverse aging and 'rejuvenate', we need to reset their immune system like the immune systems of people in their 20s," says neurophysiologist Alon Monsonego, from Ben-Gurion University of the Negev.
"However, our research shows that this might not be the case. So, one of the axioms of how to reduce aging may be incorrect."
There's a lot of scope for future research here, not least confirming that the same immune system processes are happening in humans as well as mice. The study team also wants to analyze how CD4-Eomes cell reactions might differ between people based on their genetics, their level of aging, and other factors.
Further down the line, boosting CD4-Eomes levels to increase senescent cell clearance could be an effective way of slowing biological aging and reducing some of the damage caused by inflammation later in life – but that's still some way off, and won't happen until scientists have a much better understanding of these mechanisms.
"People don't need a supercharged immune system," says Monsonego. "They need one that is working properly and appropriate for their stage in life."
The research has been published in Nature Aging.