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Projekt Druckansicht

Mechanismen der Interleukin-27 vermittelten Inhibition der Differenzierung von Th17 Zellen in der experimentellen Autoimmun-Encephalomyelitis.

Fachliche Zuordnung Molekulare und zelluläre Neurologie und Neuropathologie
Förderung Förderung von 2012 bis 2014
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 218475164
 
Erstellungsjahr 2015

Zusammenfassung der Projektergebnisse

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.

Projektbezogene Publikationen (Auswahl)

 
 

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