Research Project Outline
We recently showed dysregulation of an IL-17?triggered positive feedback loop of IL-6 signaling, which involves the activation of NF-kB and STAT3 in fi broblasts, plays a role for arthritis development in mutant mice. Because this mechanism appears to enhance experimental autoimmune encephalomy-elitis in wild-type mice, it might be a general etiologic process underlying other Th17 cell-mediated autoimmune diseases as well as chronic infl ammatory diseases. In this project, our research is focused on analyzing in vivo homeostasis of the IL-6 loop on the molecular level to identify several molecular targets to effi ciently control the enhancing level of the loop in vivo.