With high plasticity, Th17 cells play a key role in immune imbalance in sepsis, which have been shown to harbor subgroups expressing a variety of characteristic transcription factors, such as Th1-like Th17 cells specifically expressing T-bet, may producing diverse transdifferentiation outcomes under different induction conditions. The transcription factor T-bet, as driver of Th1 cell differentiation, has been shown in recent years to inhibit Th17 cells differentiation by repressing the transactivation of Rorc. Thus, T-bet expression may influence transdifferentiation of Th17 cells, especially in infectious disease models, where T-bet knockout promotes Th17 cell differentiation and enhances immune response, loss of T-bet confers survival advantage to influenza-bacterial superinfection; besides, specific knockout of T-bet in mice Th17 cells impair Th17-to-Th1 transdifferentiation, resulting in increased bacterial load in the kidneys of CLP mice. This seemingly contradictory phenomenon suggests that T-bet, as a "Bridge" molecule in Th1 and Th17 cells differentiation, may enhance protective immune response or aggravate pathological immune responses under different situations. The function of transcription factor T-bet in Th17 cell differentiation is introduced, and the special role of T-bet in immune response is discussed, this review may provide a brand new immunological perspective for sepsis and other infectious diseases.