This study investigates the role of the transcription factor GATA-3 in the inhibition of Th1 development through an IL-4-independent mechanism. The authors found that loss of GATA-3 expression in developing Th1 cells is dependent on IL-12 signaling through Stat4 and is not simply due to the absence of IL-4. GATA-3 directly represses Th1 cytokine production by a cell-intrinsic mechanism that involves repression of IL-12 signaling. This inhibition of Th1 development is mutually antagonistic with IL-12 signaling, leading to rapid dominance of one pathway during early Th development and producing a stable divergence in cytokine profiles. The study also demonstrates that GATA-3 represses IL-12 receptor β2 mRNA expression, preventing IL-12 signaling during an early developmental window. These findings provide new insights into the transcriptional regulation of Th1 and Th2 cytokine production and suggest a mechanism for the stable divergence in cytokine profiles during Th development.This study investigates the role of the transcription factor GATA-3 in the inhibition of Th1 development through an IL-4-independent mechanism. The authors found that loss of GATA-3 expression in developing Th1 cells is dependent on IL-12 signaling through Stat4 and is not simply due to the absence of IL-4. GATA-3 directly represses Th1 cytokine production by a cell-intrinsic mechanism that involves repression of IL-12 signaling. This inhibition of Th1 development is mutually antagonistic with IL-12 signaling, leading to rapid dominance of one pathway during early Th development and producing a stable divergence in cytokine profiles. The study also demonstrates that GATA-3 represses IL-12 receptor β2 mRNA expression, preventing IL-12 signaling during an early developmental window. These findings provide new insights into the transcriptional regulation of Th1 and Th2 cytokine production and suggest a mechanism for the stable divergence in cytokine profiles during Th development.