The contribution of T helper 2 (Th2) cells to the pathogenesis of neuroinflammation is underexplored. Here, the authors show that MOG35-55-specific 2D2-TCR transgenic mice lacking Itch and WWP2 in CD4 + T cells develop EAE symptoms primarily driven by Th2 trans-differentiation into pathogenic Th17 cells in the absence of IL-4. Furthermore, they identify a Jak3/STAT5/Blimp1/c-Maf axis required for the maintenance of Th2 stability by repressing Th17 genes.
- Mei Zhao
- Chao Zhang
- Yun-Cai Liu
