Researchers from a major university revealed a unique population of T cells that helps clear aging cells and maintain immune balance even at an older age, which contributes to healthier aging and prevents age related diseases.
The findings may pave the way for future treatments for aging.
Our body ages slowly, almost without noticing.
One day we feel tiredness that does not go away, a wound that heals more slowly or memory that becomes more blurred.
Behind every such change stands one complex system: the immune system, which not only protects us from disease but also determines the pace of our aging.
Now researcher reveal one of the most mysterious mechanisms in this process.
A new study published in the journal Nature Aging points to the ability of a unique group of T cells to protect the body’s tissues from the damage of time and limit the formation of tissue damage that accumulates with age.
Today we know that aging of the body is accompanied by aging of the immune system, and the way the immune system ages greatly affects the pace of aging and age related illness.
An uncontrolled or poorly regulated immune system is what leads to age related diseases.
This type of illness begins in the fourth decade of life and not only in old age as usually thought.
We are talking about ages 30 to 40.
At this time people begin to see increases in diabetes, cancer and obesity.
It is important to say this because people think aging starts late, and as a result they do not change their lifestyle earlier to avoid age related illness.
Aging is a constant struggle between damage and repair.
With age we accumulate damage in all body systems: in cells, in tissues, in organs, while systems work to repair them.
The immune system is our main repair mechanism.
When this repair system weakens, more and more damage appears and the body cannot fully fix it anymore.
As long as there is balance between damage and repair, the body stays healthy.
But when the balance is broken, damage accumulates and becomes the basis for age related diseases.
When this threshold breaks, illness begins.
It can be cancer or brain diseases such as Parkinson’s, ALS or Alzheimer’s.
It happens in all tissues.
This is why a balanced immune system is essential for healthy aging.
One reason people live longer today is that we reduced much of the damage experienced throughout life: lower exposure to pathogens, better sanitary conditions and better air quality all reduce the body’s daily burden.
Certain medications also contribute.
But even with progress, the key question is not only how long we live but how we live.
There is a big difference between aging and aging in a healthy way.
Among the people who manage to age in full health, people who reach age 100 while staying active and healthy, and super centenarians who reach 110.
There are regions people live till 120.
Insights from these regions surprisingly match the new study.
Certain immune cells found in some of these individuals seem to play a key role in maintaining immune balance at very old ages.
Three main immune cell types exist: B cells that produce antibodies, helper T cells that regulate the immune response, and cytotoxic cells responsible for killing infected or cancerous cells.
In previous work the team described changes that helper T cells undergo during aging.
During this research they found a surprising new population of helper T cells behaving like cytotoxic cells.
This discovery contradicted what was known in immunology.
At first they suspected contamination, but repeated checks confirmed a real phenomenon: a unique population of cells appearing mostly in very old age.
To test the significance of the finding, they created a mouse model in which these cells were genetically removed.
The result was clear: aging accelerated.
The mice accumulated senescent cells, cells that stop dividing but continue to act as inflammatory cells.
These cells are natural but harmful when they accumulate too much.
There is a natural mechanism that clears these cells, but it weakens with age.
The newly discovered T cells appear to clear senescent cells from tissues.
When the cells were removed, senescent cells increased greatly.
When they were present, aging slowed.
The researchers also tested whether this mechanism appears only in aging.
They created a mouse model with liver inflammation and saw that these cytotoxic like helper T cells also accumulated there at a young age during chronic inflammation.
When eliminated, senescence and fibrosis increased.
The study led to another question: why do helper T cells take on a cytotoxic role when the body already has cytotoxic cells? The answer may be that these cells have metabolic abilities that help them survive in chronically inflamed tissues.
The research, which began as an attempt to understand immune system aging, has become a bridge to future medical applications.
The scientific discussion has shifted from how to extend life to how to extend healthy life.
These findings reveal a biological mechanism that may help maintain tissue function in advanced age.
Manipulating these cells may improve quality of life and reduce age related illness in the future.
The team working on both diagnostic and therapeutic applications.
They are also conducting human research that supports these findings and will soon be published.