Using T‐cell receptor (TCR) transgenic mice, we demonstrate that TCR stimulation of naive CD4⁺ T cells induces transient T‐bet expression, interleukin (IL)‐12 receptor β2 up‐regulation, and GATA‐3 down‐regulation, which leads to T helper (Th)1 differentiation even when the cells are stimulated with peptide‐loaded I‐A^b‐transfected Chinese hamster ovary cells in the absence of interferon‐γ (IFN‐γ) and IL‐12. Sustained IFN‐γ and IL‐12 stimulation augments naive T‐cell differentiation into Th1 cells. Intriguingly, a significant Th1 response is observed even when T‐bet^–/– naive CD4⁺ T cells are stimulated through TCR in the absence of IFN‐γ or IL‐12. Stimulation of naive CD4⁺ T cells in the absence of IFN‐γ or IL‐12 with altered peptide ligand, whose avidity to the TCR is lower than that of original peptide, fails to up‐regulate transient T‐bet expression, sustains GATA‐3 expression, and induces differentiation into Th2 cells. These results support the notion that direct interaction between TCR and peptide‐loaded antigen‐presenting cells, even in the absence of T‐bet expression and costimulatory signals, primarily determine the fate of naive CD4⁺ T cells to Th1 cells.