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Activated T cells undergo metabolic reprogramming and effector-cell differentiation but the factors involved are unclear. Utilizing mice lacking DUSP6 (DUSP6^−/−), we show that this phosphatase regulates T cell receptor (TCR) signaling to influence follicular helper T (T_FH) cell differentiation and T cell metabolism. In vitro, DUSP6^−/− CD4⁺ T_FH cells produced elevated IL-21. In vivo, T_FH cells were increased in DUSP6^−/− mice and in transgenic OTII-DUSP6^−/− mice at steady state. After immunization, DUSP6^−/− and OTII-DUSP6^−/− mice generated more T_FH cells and produced more antigen-specific IgG2 than controls. Activated DUSP6^−/− T cells showed enhanced JNK and p38 phosphorylation but impaired glycolysis. JNK or p38 inhibitors significantly reduced IL-21 production but did not restore glycolysis. TCR-stimulated DUSP6^−/− T cells could not induce phosphofructokinase activity and relied on glucose …