Communication patterns may be key to multiple sclerosis treatment
Researchers at the University of Copenhagen have come closer to understanding the reason behind progressive multiple sclerosis. A new study demonstrates that the lack of proper communication between nerve cells and the immune system is determining the development of the disease, and can be the focal point for new and more targeted therapies.
The main purpose of the immune system is to protect the body against bacteria, viruses and other things that can make us ill. But sometimes the immune cells react the opposite way. Instead of protecting us, they attack the body's own cells and cause what is known as autoimmune disease. As an example, it can be seen in people suffering from multiple sclerosis.
Previous research from the Faculty of Health and Medical Sciences at the University of Copenhagen demonstrates that nerve cells can be considered a type of 'educators' of the immune cells. They tell the immune cells how to behave; therefore communication between nerve cells and immune cells is key. The same researchers have now mapped the communication pattern, which brings them closer to finding a targeted multiple sclerosis treatment.
"If the communication between nerve cells and immune cells works, nerve cells can ensure that immune cells protect the body and repair any eventual damage. If the communication does not work, immune cells begin to attack the body instead. It is therefore important that we understand the communication process and where it can go wrong," says Shohreh Issazadeh-Navikas, professor at the Biotech Research & Innovation Centre (BRIC) whose research team has conducted the new study.
Communication errors show researchers the way towards targeted treatment
Previous research by the same team has demonstrated that mice with a deficiency in the neuronal interferon beta (IFN-B) were unable to repair nerve cells. IFN-B has been used to treat patients with the autoimmune disease multiple sclerosis for many years. But this treatment has no effect for a large part of the patients, and researchers now know the reason.
"This study quite simply demonstrates that we are not treating where the problem is. Multiple sclerosis patients are treated with IFN-B, but what does not work may be located a completely different place in the ladder of the communication path. The next step is to find out how to treat each communication path station if it does not work," says Shohreh Issazadeh-Navikas.
If the neuronal IFN-B production is defective, another protein, PD-L1, will also be deficient, and the nerve cells cannot reprogramme the immune cells without it. The researchers have mapped the communication path stations between the neuronal IFN-B and the protein PD-L1. This means that the researchers can now observe how the communication goes wrong and therefore find the source of the failed communication between nerve cells and immune cells in people suffering from multiple sclerosis.
The study was conducted in a multiple sclerosis model, but it is not unlikely that the discoveries can be transposed to other autoimmune diseases such as psoriasis and type 1 diabetes.
The article "Neuronal IFN-beta-induced PI3K/Akt-FoxA1 signaling is essential for generation of FoxA1+Treg cells" has just been published in the esteemed scientific journal Nature Communications.
Shohreh Issazadeh-Navikas, email: firstname.lastname@example.org, telephone: +45 35 32 56 49
Professor Shohreh Issazadeh-Navikas
Telephone: +45 35 32 56 49