Researchers Natural killer cells show an immunological memory
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The activation of natural killer cells could play a major role in the future, especially in the treatment of cancer. In a recent study, scientists at the Ludwig Maximilian University (LMU) Munich and the University of Bonn have now decrypted a special autoimmune mechanism in the skin, demonstrating "that the so-called natural killer cells also have an immunological memory for the body's own cells."
The research team led by Professor Veit Hornung of the LMU has succeeded in deciphering the mechanism by which the immune system can attack pigmented skin cells, according to the LMU. In addition, the scientists have found that natural killer cells - contrary to the previous assumption - have a kind of memory. The results of their study, the researchers published in the journal "Immunity".
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Natural killer cells can "remember" tissue
So far, "natural killer cells have been denied having an immunological memory for the body's own tissue," reports the LMU. In the current study, it was now possible to prove that these immune cells "remember" more frequent contact with a specific contact allergen. An effect that may also be useful for therapeutic purposes. Thus, the natural killer cells could possibly be used for the prevention and treatment of black skin cancer.
Immune system attacks skin pigment cells
The pigment cells of the skin form an indispensable protective shield against UV radiation. Their effect is also evident in the popular summer tan, which can only be formed by the pigment cell enzyme tyrosinase. "The more the sun burns from the sky, the more pigments are formed by this enzyme," reports the LMU. The active ingredient monobenzone can block this enzyme and trigger a stress reaction. In this case, the immune system then attacks the affected pigment cells. A common consequence of this is the "white spot disease" (vitiligo), which leads to pigment-free areas on the skin.
Vitiligo used against skin cancer?
Earlier scientific studies have shown that people with vitiligo have a lower risk of developing the dreaded black skin cancer, explain the researchers. Thus, the active release of the disease by the tyrosinase blocker monobenzone could be a possible way to treat this cancer. "So you want to use a less serious disease as a weapon against black skin cancer," explains Dr. med. Jasper van den Boorn from the Institute for Clinical Chemistry and Clinical Pharmacology of the University of Bonn. To make this possible, however, the researchers first had to understand the mechanism by which the immune system recognizes and attacks the monobenzone-exposed pigment cells as dangerous.
Special hapten mobilizes the natural killer cells
It was known that monobenzone has a contact-sensitizing effect on the pigmented skin. The substance alone does not trigger any reaction on the skin, but "only when monobenzone docks onto tyrosinase does it form what is known as a hapten in the pigment cell, a structure that is foreign to the body and can activate the immune system," reports the LMU. In the animal model, the researchers investigated how the immune system reacts to this hapten. The result was surprising. "Normally, the immune system mobilizes a mixture of different white blood cells to attack a hapten-exposed tissue," but "multiple exposure to monobenzone only induced the natural killer cells to attack pigment cells," explains Jasper van den Boorn.
Effective immune response also against black skin cancer
As part of the immune system, natural killer cells kill abnormal cells such as cancer cells or even virus-infected cells. Physicians have assumed that they do not have an immunological memory for the body's own tissue, as it is attributed to the T and B lymphocytes. "However, our results clearly show that the natural killer cells can also provide a sustainable and effective immune response against the body's own pigment cells and thus against black skin cancer cells," emphasizes the Director of the Institute of Clinical Chemistry and Clinical Pharmacology of the University of Bonn, Professor. Gunther Hartmann.
In order to initiate the corresponding immune response, according to the LMU, "only one checkpoint had to give the go-ahead: the NLRP3 inflammasome." This is a "protein complex that, like a central site, brings together several signal information and how a switch decides whether or not immune cells and the natural killer cells receive the marching order, "explains Prof. Hornung. When this "checkpoint" was disabled, the monobenzone tyrosinase hapten did not induce the desired immune response. (Fp)