*This is a summary of the findings from the article titled "Autophagy is a critical regulator of memory CD8+ T cell formation" Further information and details on this study are located in the link below*
When an infection occurs, our immune system triggers an “aggressive reaction”: A large number of immune cells ‘called CD8+ T cells’ are produced. These immune cells recognize and remove the cells infected with the invading pathogen. The number of CD8+ T cells produced depends on the extent of the infection. Once the infection has been brought under control, most CD8+ T cells die. However, a small number of these CD8+T cells survive. These so-called "memory cells" remember the former pathogen so that they can help the immune system to react faster and more effectively if the same pathogen enters the body again.
These memory cells are also crucial for the effectiveness of vaccines. During vaccination, dead or weakened pathogens are introduced into the body. Although this does not cause infection, it allows the immune system to form memory cells able to fend off the same pathogen in the future. However, vaccines only work for people who are able to produce and maintain memory cells, which becomes increasingly difficult as we age.
In one of the most renowned scientific newspapers (eLife), a revolutionary study from Oxford has now been published. The study, led by Prof. Puleston, shows how autophagy, activated by spermidine, can restore this ability to form and maintain memory cells, which is often lost in old age.
Autophagy destroys and removes the “cell waste” and toxins that all cells accumulate over time as a result of normal cell function. The study shows that autophagy usually begins to fail in older mice. As a result, the damaged cells are no longer able to form the necessary memory cells. This is also confirmed by the fact that mice, which lack an important gene for autophagy, do not produce memory cells after infection with viruses (such as influenza).
The results of Prof. Puleston’s study shows that autophagy, which was activated with the help of the polyamine spermidine, restores the ability of older mice to form and maintain memory cells. Spermidine-treated mice developed stronger immunity to influenza after vaccination compared to other mice of similar age that were not treated with spermidine.
Early research results also show an identical picture in human immune cells. While further research is needed to elucidate the effects of spermidine induced autophagy in human immune cells, the results of this study revealed an autophagy regulatory mechanism which demonstrated the ability to reverse age-related immune senescence in humans.