Found the molecule that causes the immune cells to effectively kill the “solid” cancer

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Найдена молекула, заставляющая иммунные клетки эффективнее уничтожать "твёрдый" рак

In 2015 physicians who are struggling with cancer, has adopted a new technique: immunotherapy of cancer. The researchers found that immunotherapy can successfully work on two fronts at once – to stimulate immune cells to fight cancer and to improve the ability of antibodies that detect tumor foci.

Since then, there have been many studies that have confirmed the success of this treatment: immunotherapy, for example, won the most aggressive type of breast cancer.

Now the Scientific team from the SCRIPPS research Institute and the University of California at San Diego found that the efficacy of immunotherapy can be improved if the use of certain proteins as “switches” that direct immune cells directly to the cancer.

Explain that the Foundation of the human immune system are T-cells or T-lymphocytes. This white blood cells that, depending on their nature, are divided into T-killer cells (recognize and destroy damaged cells) and T-helper cells (amplify an acquired immune response). Previously it was shown that, activating killer T can destroy the cancer.

In the new work team under the leadership of Matthew Pipkin (Pipkin Matthew) focused on a particular type of T-killer – cells, called CD8+. They quickly and in large numbers are generated by the spleen and lymph nodes, acquire the ability to kill diseased cells, and then migrate to the source of the disease, to destroy the tumor.

However, until now it was not known as killer T learn to leave your “base” and accumulate in certain tissues. To detect the factors that cause T-killers operate outside of the lymphoid system, especially in places where the spread of the disease is not so easy. But scientists believe that the study and the acceleration of this process will increase the efficiency of immune cells.

The team found that important role in the work of T-killers plays Runx3 protein. It works with chromosomes inside T-cells: “preprogrammed” their genes so that the T cells accumulating in the tumor and other areas of rampant infection.

Understanding this mechanism is particularly important to combat “solid” tumors, since blood cancer associated with lymphoid system, T-killers and doing so very successfully, the authors note. But the tumor outside these systems, attacked by immune system is not as aggressive as I would like doctors.

To learn more about the work of the Runx3 protein, the researchers conducted tests on mice. They compared the gene expression of T cells CD8+, detected in non-lymphoid tissue, with those who were in the “General stream”. The experts used a method called RNA interference, which allows to suppress gene expression. The screening identified about ten thousand of factors that affect genes of T-killers. And the most powerful of them was the action of the protein Runx3.

“In the list of controls of T-killer cells in non-lymphoid tissues Runx3 protein is in the first place”, says Matthew Pipkin. Moreover, he found that Runx3 uses its own “genetic program” to control immune cells.

Having established this, the researchers used for their experiments a group of mice with melanoma (this type is a very aggressive cancer can be cured well with the help of immunotherapy). They tried to run the “overexpression” of a protein Runx3 or, conversely, to suppress it. As a result, in the first case the tumor growth was slowed, and survival of the animals markedly increased. In the second case the results were much worse than if the T-cells just attacked the tumor, without any “doping”.

In other words, if can enhance the activity of Runx3, a cancer cell will leave the maximum number of fighters, and the latter will win in the end.

The new data will help to significantly improve immunotherapy of cancer, researchers believe. According to them, Runx3 can be used for programming not only of “native” immune cells, but also “adopted”. So the doctors called T-cells, which are taken from the human body, is copied and multiplied in the laboratory, aimed at the destruction of a particular type of cancer, and then introduced back.

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