Fig. 7. Schematic model of Nsun2 coupling with RoRγt regulates Th17 cell homeostasis and promotes the development of colitis.

RoRγt, the key transcription factor of Th17 cell and binding to chromatin, directly recruits Nsun2 to in situ catalyze m⁵C formation on Th17-related cytokine mRNAs including Il17a and Il17f, which maintains the mRNA stability and pro-inflammatory cytokines subsequent secretion, facilitating occurrence of colitis. However, depletion of Nsun2 restrains the cell-cell communication between Th17 cells and IL-17 receptors-expressing cells, such as, enterocytes, goblet cells, neutrophils and monocytes, etc. to restrict the progression of colitis.