on March 3, 2011
The white blood cells of the immune system protects us from microorganisms that cause infections, but their excessive activation leads to the development of so-called autoimmune diseases in which organs important for the proper functioning of our body are destroyed. Examples of these diseases are type 1 juvenile diabetes, rheumatoid arthritis, Crohn’s disease, systemic lupus erythematosus and multiple sclerosis. The immune system must therefore be constantly under control and for this purpose, a certain type of white blood cells, called regulatory T lymphocytes, are responsible for the shutdown of the activation of white blood cells (immune suppression) when it becomes dangerous for our immune balance.
A group of researchers coordinated by Fabio Grassi from the IRB has found that regulatory T cells may lose their immunosuppressive identity and become very dangerous, a bit ‘like Dr. Jekyll turns into Mr. Hyde. In particular, the IRB researchers have discovered a receptor on these cells which, upon activation by a molecule present in inflamed tissues, triggers their conversion into aggressive cells only in that inflamed tissue.
The specific molecule for this receptor is the adenosine triphosphate (ATP), the power source of the cell, which in the course of inflammation is released outside the cells. Countering this action of ATP represents a new therapeutic option for autoimmune diseases that afflict more and more often the most developed societies. A future clinical trial will tell us if such a therapeutic approach could be successful in humans.
The study of the IRB researchers, published in the prestigious journal Science Signaling was made possible by funding from different foundations from Ticino and from the Swiss National Science Foundation and has shown that anti-ATP treatment results in a significant improvement of autoimmune disease through the strengthening of immunosuppressive regulatory T cells. In addition, a collaboration with a group of researchers from the University of Duisburg-Essen (Germany) permitted the dissection of the molecular network within the T cells, which is responsible for the increase of their immunosuppressive activity.
