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Mechanism of interleukin-27 mediated inhibition of Th17 cells in experimental autoimmune encephalomyelitis.

Subject Area Molecular and Cellular Neurology and Neuropathology
Term from 2012 to 2014
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 218475164
 
Final Report Year 2015

Final Report Abstract

Autoimmune diseases have become increasingly frequent in recent decades. Understanding how autoimmunity evolves is thus very important. A certain type of immune cells – termed Th17 cells – was originally thought to cause autoimmune diseases. More recently it has become clear that such Th17 cells may actually be “good” or “bad” in terms of autoimmune diseases depending on the products they produce. It was unknown how the balance between such “good” and “bad” immune cells is controlled. In my project, I discovered that a molecule, that had previously been named RBPJ, is actually required for such “bad” immune cells. Mice lacking this molecule cannot develop an autoimmune disease of the brain that models human multiple sclerosis. Also, they develop more “good” immune cells. This finding firstly helps to understand how “good” and “bad” immune cells are made and secondly may allow to treat brain autoimmune diseases in the future.

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