News & Events
T cells can be programmed to kill HIV
- December 20, 2019
- Posted by: Wiley M. Wagner
- Category: Science
HIV is a truly terrible and destructive immune disease in which a person has a significantly weakened immune system, unable to cope with even the simplest threats to health. However, at the beginning of this century, specialists studying the spectrum of immune-deficient syndromes were able to find out that among HIV patients there are less than 1% of patients whose CD8 immune cells can independently control the course of the disease and actually prevent it from spreading – it is the desire to find out what mechanisms behind it and led a team of researchers from the Pasteur Institute in Paris to a new study.
In the center of it was the theory that if artificially enhancing the properties of these same CD8 immune cells — which have a “high activity” in the “controlling” percent of patients — specialists can potentially introduce such reprogrammed cells to those patients who cannot control the course HIV syndrome. During long and very difficult studies, specialists noticed that the main difference between CD8 cells in different groups of HIV-infected people is that they can receive energy from the control group not only from glucose, but also from mitochondria enhanced in its activity.
So scientists have made several attempts to increase the mitochondria of CD8 cells so that they can effectively fight infected T-cells like CD4, which spread the disease. As a reprogrammer, they used interleukin-15, a special secretion of the immune system, and managed to achieve impressive results.
In fact, scientists were able to efficiently and without any special problems reprogram CD8 immune cells in ordinary HIV patients in such a way that, with the help of interleukin-15 and individual molecular processes, the enhanced mitochondria work can be started. As a result, a significant proportion of patients who have implanted genetically modified T cells began to show a significant degree of relief of their condition.