Abstract The involvement of regulatory and suppressive B cell has been mostly associated with control of autoimmune responses; and their role in cancer escape remains unknown. Recently we reported the existence of a unique subset of B cells that suppress T cell responses to promote lung metastasis of breast cancer. These cells, designated as tumor-evoked B cells (tBreg), were actively generated by tumor cells from normal B cells. Interestingly, number of FoxP3+ Tregs was also enhanced in tumor-bearing mice, although the mechanism of Treg expansion remains unknown. We hypothesized that tBregs induce the generation of Tregs. Utilizing in vitro and in vivo approaches, we demonstrate that tBregs indeed induce the generation of FoxP3+ Tregs from resting CD4+ T cells. The molecular mechanism of this process is that tBregs abundantly express and utilize TGFb. The generation of FoxP3+ Tregs is blocked by selective inhibition of the TGFb receptor signaling, such as by the use of TGFb-type I receptor-like kinase ALK5 inhibitor. Importantly, the tBreg-induced FoxP3+ Tregs promote lung metastasis, as proved by their adoptive transfer in NOD/SCID mice. Taken together, our data indicate that tBregs facilitate lung metastasis by inducing Tregs in a TGFb-dependent manner. Thus, the clinical implications of our findings are that, to effectively combat cancer and its metastasis, tBregs have to be controlled to interrupt the initiation of cancer-induced suppressive events.