Fig. 7: Schematic showing the molecular mechanisms by which Neat1 regulates antigen-specific Th17 cell responses in EAU.

The increased expression of Neat1 is induced by IL-23 signaling, and Neat1 in turn augments IL-23R expression by regulating NonO and miR-128-3p/NFAT5, thus forming a positive feedback loop to sustain antigen-specific Th17 cell responses that contribute to the progression of EAU.