Involvement of lncRNA-1700040D17Rik in Th17 cell differentiation and the pathogenesis of EAE

- A novel lncRNA, 1700040D17Rik, was found to be down-regulated in EAE model.
- After the treatment of rhIL23R-CHR, 1700040D17Rik was significantly increased.
- 1700040D17Rik was revealed to associate with the differentiation of Th17 cells.
- 1700040D17Rik was confirmed to regulate RORγt to affect Th17 cells.

IL-23/STAT3 signaling pathway is a key process in Th17 cell differentiation, and Th17 cells are closely related to the development of autoimmune diseases. We previously designed and prepared rhIL23R-CHR protein to antagonize endogenous IL-23, showing effectiveness in the treatment of experimental autoimmune encephalomyelitis (EAE) in mice. To further elucidate the mechanism of action, mouse lncRNA microarray was used to screen expression profiles of lncRNAs, and a particular lncRNA, 1700040D17Rik was found to down-regulate in EAE model and its expression was significantly increased after the treatment by rhIL23R-CHR. The function of 1700040D17Rik was revealed to associate with the differentiation of Th17 cells through the regulation of the key transcription factor RORγt. Together, regulation of Th17 cells through lncRNA is responsible for the effects of rhIL23R-CHR to balance the immune responses, and 1700040D17Rik has the potential to serve as a therapeutic target or a biomarker for autoimmune diseases.