There are some studies about anti-aging proteins that have long been shown to protect against age-related diseases, such as cancer, neurodegeneration, and cardiovascular disease. Those proteins are present in the blood, and they can be measured to get an idea of the metabolism of your body.
The immune system is an army to defend or organism from the external agents that cause many diseases. As all other systems in our body, the immune system gets old and its functioning decreases with age.
There is a study by researchers at the Gladstone Institutes now reveals that one such protein could also be targeted to rejuvenate cells in the immune system.
The protein that they studied is called SIRT1. Human sirtuins (SIRT1–7) are highly conserved proteins that regulate cellular processes linked to metabolism and organismal longevity. In the new study, the scientists found that it is also involved in how cells in the immune system develop with age, specifically the cytotoxic T cells. These cells are highly specialized guardians of the immune system and their role is to kill cells infected by a virus, damaged cells, or cancer cells. With the course of life, these T cells mature and eventually lose a protein called CD28 and as these cells get older, they become more toxic to their environment.
What happens when the cells get old?
At the time a young T cell is inactivated, it uses oxygen to stay in its resting stage. Once it is needed to defend the body against a bacteria or virus, it turns on an activated stage and initiates glycolysis and uses sugar to get an immediate boost in energy and produce cytokines. As the cells age and lose CD28, they can shift into glycolysis much more quickly if the resting stage is inhibited. They also lose the anti-aging protein SIRT1. That makes them more toxic to the cells around them.
In the new study, Ott and her team studied human T cells, isolated from blood donors of all ages, to compare mature cytotoxic T cells with young ones.
They found that naive T cells have a high concentration of SIRT1. This stabilizes an entire mechanism that prevents the cells from entering glycolysis to use sugar as an energy source, and limits their toxic effects, by decreasing the production of cytokines and all the inflammatory processes.
This information could lead to the production of medicine targeting the strengthening of SIRT1 in mature T cells or keep them from progressing too quickly into a highly toxic state, and could postpone the development of age-related diseases. On the other hand, those drugs could be used to encourage the T cells to be more toxic by temporarily making young T cells more aggressive, they could, for example, support an aggressive anti-tumor response or other immune therapy.
Mark Y. Jeng, Philip A. Hull, Mingjian Fei, Hye-Sook Kwon, Chia-Lin Tsou, Herb Kasler, Che-Ping Ng, David E. Gordon, Jeffrey Johnson, Nevan Krogan, Eric Verdin, Melanie Ott (2018). Metabolic reprogramming of human CD8 memory T cells through loss of SIRT1. The Journal of Experimental Medicine. Retrieved from: https://rupress.org/jem/article/215/1/51/42488/Metabolic-reprogramming-of-human-CD8-memory-T
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