Ancient and modern, both at home and abroad, are exploring how to make people live forever. If you want to live forever, you must figure out why people get old? A recent new study suggests that it may provide some ideas.
As a kind of immune cell, T cells are used to protect us from pathogens, but a new study shows that they may also accelerate the body’s aging. Blocking the inflammation caused by cells or increasing the supply of key metabolic molecules can reduce the severity of certain aging-related symptoms in rodents. These methods may be beneficial to delay aging.
As we age, our T cells will make us sick and weaken our resistance to pathogens. This decline in resistance may explain why the elderly are more susceptible to infection. As we age, one reason T cells begin to age is the weakening of the activity of mitochondria (the devices that provide energy within the cells).
But the activity of T cells may not only reflect aging. From the cellular level, the elderly have chronic inflammation all over the body, and researchers have suggested that inflammation will accelerate aging. T cells may be involved in this process because they release molecules that stimulate inflammation.
To test this hypothesis, immunologist María mittelbrun and his colleagues genetically modified mice to make the mitochondria of T cells lack protein. This change forces the cell to switch to a low metabolic efficiency state to obtain energy.
Researchers reported in the journal Science that when these rodents are 7 months old, it is usually the golden age of their lives for mice, and they appear to be aging. Compared with ordinary mice, mice after genetic modification are slower. Their muscle atrophy became weak, and their resistance to infection declined. This is like many elderly people, their heart function declines, and a lot of body fat is lost.
The research team found that the modified mouse T cells secrete molecules that trigger inflammation, which suggests that T cells may be part of the cause of animal body degradation. Mittelbrunn said: “The immune system plays a role in promoting the speed of aging.”
The scientists also tested whether they can slow the rate of aging. First, they injected mice with a drug to block tumor necrosis factor alpha (TNFα), which is an inflammation-inducing molecule released by T cells; this method increased the animals’ grip strength and improved their performance in the maze , And enhance the pumping capacity of the heart.
Mittelbrunn and his colleagues also gave these animals a compound that raises levels of nicotinamide adenine dinucleotide (NAD), a molecule that is essential for metabolic reactions and enables cells to extract energy from food. The concentration of NAD in cells usually decreases with age. Researchers have found that increasing the concentration of NAD in mice makes them more active and enhances heart function.
However, other researchers questioned the relevance of this result to normal aging. As the biologist Nafdeep Chandel of Feinberg School of Medicine at Northwestern University points out, the mitochondria of genetically modified mice are much more damaged than the mitochondria of many elderly people. He said, “For most of us, I bet our T cells are fine.”
However, T cells with mitochondrial dysfunction may cause senescence in some people who seem to age prematurely and develop age-related diseases at a relatively young age.
Judith Campisi, a molecular cell biologist at the Buck Institute for Aging, agrees. She said, “This research has set a new milestone in understanding how the immune system changes with age, but I don’t know how much it accelerates natural aging.”