Publication date: Sep 04, 2019
A molecule that regulates the production of IL-17 in Th17 cells, called retinoic acid t (RORγt), has caught scientists’ attention before as a potential target for treating autoimmune diseases. Their work showed that REV-ERBα, a molecule known to suppress the activity of RORγt by competing in a variety of processes for the same binding site on the DNA of cells, also competed for that site with Th17 cells. When the team specifically increased the levels of REV-ERBα in Th17 cells grown in the lab, both RORγt activity and Il-17 production were suppressed. -REV-ERBα is induced during Th17 cell differentiation and directly competes with RORγt by binding to [specific] sites to repress the expression of key Th17 cell signature genes,” the scientists wrote. Researchers believe their work suggests that boosting REV-ERBα activity through SR9009 lowers inflammation, and without harming the immune system in ways that current RORγt suppressive efforts do.
|disease||MESH||experimental autoimmune encephalomyelitis|
|pathway||BSID||Th17 cell differentiation|