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The mechanism by which the leprosy pathogen blocks the immune response has been deciphered
Last reviewed: 01.07.2025
The pathogen of this terrible disease suppresses the activation of the immune system by vitamin D: instead of running away or hiding from the watchful eye of the immune system, the bacteria seem to order the immune cells to “lay down their arms.”
While some bacteria hide from the immune system with clever camouflage, others avoid attack by hijacking the immune system's controls. We are talking about Mycobacterium leprae, the causative agent of leprosy.
Although leprosy is associated in the common consciousness exclusively with the "dark middle ages", it has successfully survived to this day: in 2008, for example, 249 thousand new cases were registered. Scientists have managed to thoroughly study the symptoms and ways of development of the disease over several centuries, but how leprosy manages to thrive despite the efforts of the immune system has remained a mystery until now.
Researchers from the University of California, Los Angeles, have managed to decipher the molecular mechanism by which M. leprae blocks the immune response. It turned out that in this case, so-called microregulatory mRNAs are at work. These are very short molecules that, like all RNAs, are synthesized on DNA, but do not carry any information about proteins. Instead, they are busy regulating the work of other encoding RNAs. MicroRNAs bind to the messenger RNA encoding a specific protein and suppress protein synthesis on it.
Scientists compared how two types of infection develop: the milder tuberculoid leprosy and the more aggressive, body-wide lepromatous leprosy. They found that these types differed in 13 microRNAs synthesized by the bacteria. Those RNAs, which were more abundant in the more severe form, targeted genes that control immunity, including the activity of macrophages and T-lymphocytes.
Activation of the immune response depends on vitamin D; its deficiency in the body contributes to the development of chronic infections and autoimmune diseases. One of the microRNAs, hsa-mir-21, suppressed the synthesis of the protein responsible for the activation of immunity by the vitamin. As soon as the activity of the microRNA itself was suppressed in macrophages, these cells immediately regained the ability to eat bacteria. As the researchers write in the journal Nature Medicine, without the saving microRNA, the survival rate of the leprosy pathogen decreased fourfold. Moreover, leprosy helps any infection in general, and not just itself: scientists have shown that immune cells with the leprosy microregulatory RNA thrown into them (it appears there 18 hours after the appearance of the pathogen) stop responding to the tuberculosis pathogen. Leprosy, instead of running away and hiding from the immune system, seems to order it to lay down its arms.
Although this method of “avoiding responsibility” by subordinating immune commands seems quite clever, the researchers believe that neutralizing this mechanism will not be difficult: it is enough to combine the neutralization of microRNA with an increased dose of vitamin D. At the same time, they do not exclude that many diseases associated with immune disorders, including cancer, occur not so much due to a lack of vitamin D, but due to the inability of immune cells to respond to it. Perhaps in this case, the cure for leprosy could be useful in combating a whole range of immunological disorders.