Suppress the uprising
The Japanese have found out the mechanism of the immune system cells getting out of control
Dina Mingalieva, Copper News
The immune system is a magical defense against microbes, identifying and destroying threats with the help of an extremely complex adaptive network of special cells. However, a system of such mind-boggling complexity can fail. For example, due to genetic mutations, some of these cells can get out of control: they stop distinguishing between threats and your own cells and start attacking healthy tissues and organs. This can lead to the development of autoimmune diseases – for example, arthritis, inflammatory bowel diseases, type I diabetes and many other common health difficulties.
Most modern methods of treating autoimmune diseases involve blocking important elements of the immune system, which makes the patient vulnerable to potentially dangerous bacterial and viral infections. Scientists have not yet been able to identify the mechanism of these rebellious cells. However, researchers from the Okinawa Institute of Science and Technology (OIST) have uncovered a previously unknown role of a well-known molecule called JunB and its associated gene: JunB is of key importance in disrupting the functioning of a special type of white blood cells. The results of the study are published in the journal Nature Communications (Hasan et al., JunB is essential for IL-23-dependent pathogenicity of Th17 cells – VM).
The team studied T-helper white blood cells, which coordinate the immune system's response by producing a range of communication signals in the form of molecules called interleukins. JunB functions in T helper cells 17, a subtype that is responsible for the initial immune response to infection. Sometimes these T-helpers 17 get out of control and become toxic to the intestines and joints of a person.
"There are a lot of T-helpers in our intestines 17. They play three roles in our body. Firstly, they support intestinal health, and secondly, they deal with bacterial and fungal infections. Thirdly, their toxicity leads to autoimmune diseases, which we would like to avoid," EurekAlert quotes the head of the study, Professor Ishikawa.
A team from Okinawa has studied the process by which T-helpers 17 become toxic. One of the communication molecules of the immune system – interleukin-23 – should "wake up" T helper cells 17 during infection and force them to fight the invasion. However, interleukin-23 is a double–edged sword: it sometimes provokes these T-helpers to get out of control. In order for T-helpers 17 to hear the call to action, they need to reflect interleukin-23 receptors on their surface, which means activation of the corresponding gene – usually "turned off". Finding a way to prevent this gene from being activated is a potential opportunity to stop this whole process. And that's where JunB comes on the scene.
JunB is a transcription factor, it regulates – turns on and off – the activity of a gene or group of genes in the DNA of a cell. Scientists identified JunB by systematically checking transcription factors in the DNA of the T helper 17 cell. To this end, they took turns "cutting out" – breaking the DNA sequence – the genes for each transcription factor. Each time, the scientists checked whether T-helper 17 reflected its interleukin-23 receptors. After shutting down JunB, they found that T-helper 17 no longer reflected interleukin-23 receptors and could not get out of control. Moreover, mice whose T-helpers did not produce JunB did not develop autoimmune diseases associated with T-helpers 17.
Drawing from the OIST Subduing the Rebellion press release:
Unmasking Rogue Cells in the Immune System – VM.
It took the researchers two years to get a mouse model with JunB disabled.
The most interesting thing is that T–helpers 17 without JunB are still able to accumulate in the intestine and fight infections. If scientists can develop a drug that will fight JunB directly, it can prevent T helper 17 cells from getting out of control without negatively affecting the entire immune system.
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31.05.2017