The reduced iTh17 and enhanced iTreg polarization of DUSP4-/- CD4 T cells thus link DUSP4 deficiency with altered Th cell development, and provide a mechanistic explanation for the enhanced resistance to autoimmune encephalitis; results from the exogenous IL-2 and anti-IL-2 antibody treatments further suggest IL-2 signaling, but not IL-2 secretion per se, are likely involved in this scenario. The gene discussed is DUSP4; the disease is autoimmune encephalitis.