How temperature controls Immunity
Temperature sensitivity helps the immune system to fight a variety of diseases
Kirill Stasevich, "Science and Life", based on the materials of the University of Warwick: Hotter bodies fight infections and tumours better – researchers show how
When an infection or tumor appears in the body, immune cells adjust the activity of their own genes so that they eliminate the threat with maximum efficiency.
To do this, special proteins are sent to the cell nucleus, which recognize the necessary genes in DNA, bind to them and force other proteins to synthesize matrix RNA more actively on the genes. The synthesis of RNA on DNA is called transcription, and the proteins that regulate it are called transcription factors. Then the RNA copies are picked up by other molecular machines that synthesize the necessary proteins on them.
One of the most well–known regulators of immune gene activity is a transcription factor called the nuclear factor "kappa-bi", or NF-kB (here it should be clarified that NF-kB is not the name of a single protein, but of a whole family). However, the work of NF-kB is not limited to coming to the cell nucleus, turning on immune genes and sitting on them until the victorious end.
In fact, it behaves like a pendulum, then coming into the nucleus, then leaving it; accordingly, the immune genes controlled by Kappa-bi are switched on and off. If the cycle is broken, if the "kappa-bi" is unregulated and, coming to the core, will stay there longer than usual, then the inflammatory reaction will get out of control, and autoimmune diseases such as psoriasis, rheumatoid arthritis, etc. may begin.
Moreover, the NF-kB itself has its own regulators. Researchers from The University of Warwick writes in their article in PNAS (Harper et al., Temperature regulates NF-kB dynamics and function through timing of A20 transcription) that the kappa-bi travels through the cell depend on temperature: the higher it is, the more often it runs to the nucleus and back. And the rhythm of its work depends on another immune protein called A20.
Figure from the article in PNAS – VM
It is known about A20 that it soothes the immune system by suppressing inflammatory processes. If the cell was deprived of A20, then the "kappa-bi" in it stopped feeling the temperature. Here we can remember that our body temperature changes during the day: the biological clock cools us slightly during sleep.
Although the daily temperature fluctuations are not very large, within one and a half degrees, "Kappa-bi" feels such fluctuations, according to the authors of the work. And those problems with immunity, such as uncontrolled inflammation, that occur in people with an upset biological clock, can occur precisely because a broken clock causes a disorder in temperature cycles, which, in turn, affects the work of the immune regulator NF-kB.
On the other hand, it is known that if mice are kept at a temperature higher than usual, they will be more resistant to malignant diseases, and they will tolerate inflammation more easily; and infections like influenza or the common cold are more severe in the cold season. (And we have already written once that our immune genes work differently in summer than in winter.)
Obviously, all this can be explained by the sensitivity of the immune system to body temperature and the environment: in a warm environment, thanks to more frequent kappa-bi cycles, the immune system copes with problems better. And, perhaps, such temperature sensitivity can be used in the treatment of a variety of diseases, from colds to cancer.
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