The malaria parasite makes the immune system forget about its existence
Last reviewed: 20.11.2021
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The malarious plasmodium causes immunity to forget about its existence: the parasite interferes with the development of lymphocytes, depleting the reserve of memory T-cells, which just have to remember the pathogens "in person".
Perhaps the most surprising and most unpleasant property of malaria can be called the ability of its pathogen to escape from the immune attack. Many studies have been devoted to the relationship between malarial plasmodium and the immune system. One of the plasmodic tricks is the ability to literally hide from immune intelligence. Another way, which is written in the journal PNAS researchers from Yale (USA), is to reprogram the parasite of the host's immune cells.
It is known that a malarial parasite causes severe inflammation, which can lead to severe complications if, for example, the spinal cord is affected. Scientists have found that inflammation of this plasmodium provokes itself with the help of the PMIF protein, which is extremely similar to one of the signaling proteins-cytokines of the immune system. This protein causes the undifferentiated T cells to turn into T-killers, designed to attack and kill the disease. It would seem, what is the benefit? But in this way plasmodium depletes the store of T-memory cells. The function of these cells is to memorize the pathogen and, during its repeated visit, to intentionally set the immune system against it in accordance with the available "dossier".
T-cells of memory live for a long time (unlike T-killers), and thanks to them they often manage to avoid a serious war with the pathogen: immunity neutralizes it even before it comes into full force. Not that with malaria: they simply do not form. All resources are spent on the production of T-killers. As a result, each subsequent attack of the disease is the first, and no immunity is produced.
Obviously, when developing a vaccine, one can not ignore this ingenious ability of the pathogen of malaria.