This is how cancer cheats the body’s defenses


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PD1 protein has the role of moderating the response of the immune system to harmful agents. However, it is also the weak link that cancer cells take advantage of to escape lymphocyte action. The finding allows us to understand how to attack the problem and develop more effective treatments against cancer.

The human body defends itself against potentially harmful cells with a response activated by leukocytes T. This immune system response is in turn controlled by the PD1 protein. Cancer cells take advantage of the function of this protein to camouflage, go unnoticed and multiply.

Now, a team of researchers from the German universities of Freiburg and Hanover they discovered how the protein that allows this escape mechanism is activated.

How the body defends itself from cancer

Cancer cells (reference image)

T lymphocytes or T-cells meet An important function for the immune system. Are the cells that activate and regulate the body’s defense. To trigger this response from the immune system, the intervention of a cell that has antigens (CPA) is necessary. CPAs comprise dendritic cells, leukocytes and macrophages, among others.

When a CPA “presents” an antigen or a potentially carcinogenic cell to T lymphocytes, they are activated to initiate the attack against the threat or in turn activate leukocytes or macrophages for it.

How cancer cells deceive the body

Occasionally, cancer cells evolve in such a way that they find a way to camouflage and escape the body’s immune response. This is due to the action of the PD1 protein found in T lymphocytes. PD1 regulates and moderates the immune system response, since it stops the reaction processes of the organism and the destruction of other healthy cells (as could happen in an autoimmune disease). Cancer cells take advantage of the action of PD1 to multiply and go unnoticed.

The researchers from Hannover and Freiburg discovered that cancer cells activate by a signal to the protein tyrosine phosphatase 2 (SHP2) that binds to the PD1 of T leukocytes at two specific points. This finding would allow the development of a specific medication to avoid the union between SHP2 and PD1 and generate autoimmune responses of the organism. The study was published in the scientific journal Science Advances.


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