Around 2.5 million people are affected by the autoimmune disease Multiple Sclerosis (MS), the commonest central nervous system disease among young adults. There are around 12,500 MS sufferers in Austria and 400 new cases every year. There is currently no cure for MS but, with appropriate treatment, it is possible to delay the typical progression of the disease. In collaboration with national and international groups in Japan, Germany and Switzerland, researchers from MedUni Vienna, led by Wilfried Ellmeier from MedUni Vienna’s Institute of Immunology, have now discovered in an animal model that the family of histone deacetylases (HDACs) plays a major role in the development of this type of autoimmune disease. After the necessary follow-up studies, this could lead to a new approach to treating Multiple Sclerosis in the future.
Background: The human immune system is based on a lively exchange of information between the cells, allowing for a coordinated response to germs or pathologically modified cells. This process requires the DNA information contained in the cells to be read and this is often regulated by so-called “epigenetic” processes (i.e. via the “degree of packaging” of the DNA). Special enzymes, the family of so-called histone deacetylases (HDACs), play an important role in this process. In total there are 18 different HDACs. They determine the “degree of packaging”, that is to say how efficiently the information can be read.
If the “degree of packaging” is lessened, it is easier to read the DNA, and this controls the expression of a large number of proteins. In addition to this, HDACs can also regulate the activity and function of proteins. This then leads to an increase in cell activity and boosts communication between the immune cells. In the immune system, increased cell activity during an immune response is primarily manifested by an increase in the number of special immune defence cells, T-cells (or T-lymphocytes). The extent of an immune response is thereby regulated by the HDAC family.