Teilprojekt A15N

Leider keine deutsche Projektbeschreibung vorhanden.

IL-17-producing T helper cells (Th17) have been identified recently as a subpopulation of CD4+ T cells. Besides having a protective function in the defense against extracellular bacteria and fungi, they also play an important role in autoimmunity and chronic inflammation. They form the major fraction of pathogenic T cells in experimental autoimmune encephalitis (EAE), a mouse model of multiple sclerosis, and they have also been shown to play a role in the pathogenesis of inflammatory bowel disease (IBD).
A series of signals controlling the differentiation of this subset in vitro have already been identified. However, it remains enigmatic how the control of this pro-inflammatory cell population occurs in vivo. In our preliminary work we were able to identify the gut as a crucial organ for homeostatic regulation of this subset. Th17 cells are controlled by two different ways in the small intestine: first, pro-inflammatory T cells are eliminated via the intestinal lumen. Simultaneously, Th17 cells can be reprogrammed and converted into regulatory CD4+ IL-17A+ T cells with immunosuppressive and regulatory
properties (rTh17).
These findings may have impact for future therapeutic manipulation of the pro-inflammatory Th17 cell population in autoimmune diseases. However, this first requires a more detailed analysis of the mechanisms controlling the in vivo function of the Th17 cell compartment. This project aims to identify the mechanisms underlying the elimination and reprogramming of Th17 cells in the small intestine.