From fire to fire: how chemotherapy creates autoimmune inflammation
Last reviewed: 23.04.2024
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Antineoplastic medications give a signal to the synthesis of immune receptors that regard the damaged DNA of tumor cells as a "signal to fight" and begin a "protective" inflammatory reaction.
Deficiencies in DNA can provoke an immune response and an inflammatory response, according to researchers from the National Institutes of Health (USA). In their work, they found that chromosome damage stimulates cell production of so-called tol-like receptors, whose function, generally speaking, is the recognition of bacteria and other foreign agents.
Nevertheless, these receptors are able to bind to the legendary anti-tumor protein p53 (it is often called the "guardian of the genome"). The protein reacts to tumor degeneration and initiates in apoptosis malignant cells the processes of apoptosis - "programmed suicide", triggering the synthesis of mRNA (transcription) on the genes of "suicidal" enzymes. Moreover, such interaction of immune receptors and p53 was characteristic only for primates.
The researchers worked with samples of human blood, from which the white blood cells were taken. The latter were treated with anti-cancer drugs to activate the synthesis of the p53 protein. As a result, together with p53, the cells also began to develop immune receptors, albeit with different activity in different blood samples. And the appearance of receptors could be suppressed with a p53 protein inhibitor pifitrin. Obviously, p53, as in the case of apoptosis, is directly involved in the activation of receptor genes.
The article with the results of the research is published on the PLoS Genetics website.
The immune response is always associated with the invasion of foreign agents. Therefore, the whole work may seem strange and incomprehensible biochemical tricks - if not for the fact of inflammation in many patients after chemotherapy. The explanation of such an organism response to treatment can be as follows: most anti-cancer drugs "beat" the DNA of cancer cells. Destroyed DNA is perceived as a foreign agent and includes an immune response with all the inflammatory effects. The difference in the level of synthesis of immune receptors in different blood samples is explained, therefore, by the individual sensitivity of the immune system to DNA damage.
Deciphering the mechanism of interrelation of tumor and immune processes will help not only to facilitate therapy of oncological diseases, but also to understand the nature and methods of fighting autoimmune inflammations.
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