Murine Foxp3+ Treg have recently been shown to express T‐bet, a transcription factor characteristic of Th1 effector cells. A human Treg phenotype equivalent has not been reported. Here, we show that naïve human CD4+ T cells incubated with low numbers of CD40‐activated allogeneic B cells preferentially differentiate into alloantigen‐specific CD4hiCD25hi Treg. These differentiated cells potently suppress effector T‐cell responses and express T‐bet, IFN‐γ, and CXCR3, the features of Th1 effector cells. In contrast, co‐culture of naïve CD4+ T cells with high numbers of allogeneic B cells results in CD4+CD25+ T cells that promote, rather than inhibit, effector T‐cell responses, demonstrating the plasticity of CD4+ T‐cell differentiation in response to alloantigen‐presenting B cells. The optimal accumulation of CD4hiCD25hi Treg induced using higher T cell:B cell co‐culture ratios was dependent on the expression of T‐bet and endogenously produced IFN‐γ. Induction of Treg‐mediated suppression function in the Treg population was not. As CXCR3 confers the preferential trafficking of T cells to tissue sites of IFN‐γ, these human Th1‐like Treg might be useful for modulating pathological Th1 effector responses, such as that occurring during graft‐versus‐host disease or graft rejection.