Although Th17 cells are critical to host protection at epithelial barriers, such as the skin, they also play a pathogenic role in inflammatory and autoimmune diseases. Glucocorticoids (GC) are frequently used to suppress undesired inflammation in such conditions. Interestingly, Th17 persistence under GC therapy is not uncommon, which is often explained by a GC-refractory character of these cells. Several studies reported however increased serum levels of IL-17 and circulating Th17 cells in GC-treated compared to GC-untreated patients, which cannot be explained by GC insensitivity, but rather implies a stimulatory effect of GCs on Th17 responses. In this project, we are investigating whether GC are able to induce human Th17 cells and the potential mechanisms involved.
GC are extensively used to treat allergies, auto-immunity and auto-inflammation, in which Th17 cells play an important pathogenic role. Moreover, long term use of GC compromises host defense at barrier sites and thereby increase the risk for infections. Knowledge of the molecular mechanisms underlying the GC regulation of Th17 cells is important for advancing immunosuppressive therapies to balance inhibition of T-cell-driven inflammation and preservation of Th17-mediated host defense in inflammatory diseases.
Dept. of Dermatology / RG location - LFI Building
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