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Out of the fire and into the fire: how chemotherapy creates autoimmune inflammation
Last reviewed: 30.06.2025
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Antitumor drugs signal the synthesis of immune receptors, which regard damaged DNA of tumor cells as a “signal to fight” and begin a “protective” inflammatory response.
DNA defects can trigger an immune response and an inflammatory reaction, according to researchers at the National Institutes of Health (USA). In their work, they found that chromosome damage stimulates the cell to produce so-called toll-like receptors, whose function, generally speaking, is to recognize bacteria and other foreign agents.
However, these receptors are capable of binding to the legendary antitumor protein p53 (often called the "guardian of the genome"). The protein reacts to tumor degeneration and initiates apoptosis processes in malignant cells - "programmed suicide", starting the synthesis of mRNA (transcription) on the genes of "suicidal" enzymes. Moreover, such interaction of immune receptors and p53 turned out to be characteristic only of primates.
The researchers worked with human blood samples, from which leukocytes were selected. The latter were treated with anti-cancer drugs to activate the synthesis of the p53 protein. As a result, along with p53, the cells also began to develop immune receptors, although with different activity in different blood samples. Moreover, the appearance of receptors could be suppressed by the p53 protein inhibitor pifithrin. Apparently, p53, as in the case of apoptosis, is directly involved in the activation of receptor genes.
An article with the research results was published on the PLoS Genetics website.
The immune response is always associated with the invasion of foreign agents into the body. Therefore, all the work may seem strange and incomprehensible biochemical tricks - if not for the fact of inflammation in many patients after chemotherapy. The explanation for such a reaction of the body to treatment can be as follows: most anti-cancer drugs "hit" the DNA of cancer cells. Destroyed DNA is perceived as a foreign agent and includes an immune response with all the inflammatory consequences. The difference in the level of synthesis of immune receptors in different blood samples is thus explained by the individual sensitivity of the immune system to DNA damage.
Deciphering the mechanism of the relationship between tumor and immune processes will help not only to facilitate the treatment of oncological diseases, but also to understand the nature and methods of combating autoimmune inflammation.
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