Scientists in Mainz and Zurich have contested a popular hypothesis concerning the emergence of multiple sclerosis
Interleukin 17 proteins appear to play no essential role in the emergence of autoimmune diseases of the brain like multiple sclerosis
During an autoimmune disease, the endogenous defence system (the immune system) loses the ability to distinguish between "self" and "foreign". As a consequence, the immune system directs its defence against itself, with fatal consequences. In the case of multiple sclerosis, a chronic, inflammatory autoimmune disease, the immune system attacks the protective layer encapsulating the nerve fibres: This protective layer formed by myelin works like insulation for electrical cables. If the insulation is damaged, the nerves can no longer transmit messages effectively.
In the emergence of certain autoimmune diseases so-called T helper cells play a decisive role; like the small proteins called cytokines, which they produce. In particular, ’Th17’ cells which were discovered only few years ago as a subclass of the T helper cells. Their presence at the emergence of autoimmune disease like multiple sclerosis has been the object of numerous publications within the last three years. The Th17 cells are named after the cytokine Interleukin 17 (IL-17), which they produce in large amounts. Therefore, it was easy to assume that the emergence of MS was linked to the function of this molecule. Particularly, the two main proteins of the Interleukin 17 family, namely IL-17A and IL-17F, moved into the spotlight of many researchers.
In a collaborative study, researchers in the laboratories of Professor Ari Waisman at the Mainz University Medical Center and of Professor Burkhard Becher at the Institute for Experimental Immunology of the University Hospital Zurich together with colleagues from Berlin and Geneva examined the direct effects of those two cytokines on the development of "EAE" in mice. This disease is comparable with the MS in man on many levels and therefore serves an animal model for MS. On the one hand the researchers could point on that mice not producing one of the two cytokines, are just as susceptible to the emergence for EAE as "normal" mice. On the other hand the specific overproduction of the two cytokines in the brain did not lead to a higher vulnerability for MS-related disease either. Interestingly, the increased production of the cytokine in the whole body of the mice led to inflammations in a variety of organs, primarily in the skin. This shows that IL-17 can be a harmful cytokine, but not necessarily in connection with autoimmune diseases of the brain.
"The result that neither IL-17A nor IL-17F play a decisive role in the emergence of the EAE was a great surprise for us", stated Professor Ari Waisman of the Department of Internal Medicine I. "This will supposably lead to change among experts because we could not confirm a popular hypothesis with that. The results of the current study are, however, very important for the development of future treatment strategies of autoimmune diseases of the brain. In connection with MS the focus should be taken away from the Interleukin 17 and placed on other cytokines."