It is estimated that nearly 1 million Americans suffer from multiple sclerosis (MS), an autoimmune disorder characterized by chronic inflammation. To date, doctors are still not sure as to what causes MS; however, new research offers a new viewpoint on this subject.
The Same But Different
This study was conducted by a team from the University of Zurich, and based its findings on 61 pairs of monozygotic twins, commonly known as identical twins. For each of these sets of twins, one had been diagnosed with MS, while the other had no history of this condition.
Once the twins had signed up, the research team took a close look at the immune systems of each subject. To do this, the study authors relied on a relatively unique approach, as expressed by Florian Ingelfinger, of the contributors to the study. “We use[d] a combination of mass cytometry and the latest methods in genetics paired with machine learning to not only identify characteristic proteins in the immune cells of the sick twin in each case, but also to decode the totality of all the genes that are switched on in these cells,” stated Ingelfinger in a University of Zurich press release.
An Overactive Immune System
Given the fact that the researchers examined identical twins, the authors could successfully rule out genetic factors when documenting changes to the immune system. Instead, the team noted that what separated the subjects with MS from those without this condition was cytokine receptors. “Surprisingly, we found the biggest differences in the immune profiles of MS affected twins in to be in the cytokine receptors, i.e. the way immune cells communicate with one another. The cytokine network is like the language of the immune system,” stated Ingelfinger.
Essentially, what the team found was that subjects with MS had immune systems that were more sensitive to certain types of cytokine cells. In turn, this caused an increased activation of another type of immune system cell in the bloodstream, known as T cells. All of these extra T cells could very well make their way into the body’s central nervous system, thereby causing symptoms associated with MS.
“The findings of this study are particularly valuable in comparison to previous studies of MS which do not control for genetic predisposition,” stated Burkhard Becher, a professor at the Institute of Experimental Immunology at the University of Zurich. “We are thus able to find out which part of the immune dysfunction in MS is influenced by genetic components and which by environmental factors. This is of fundamental importance in understanding the development of the disease.”
