Despite growing evidence highlighting the relevance of increasing IL-10-producing B cells (B10cells) in autoimmune diseases, their functions in patients are still unknown. The aim of this study was to evaluate the functions of CpG-induced B10 cells isolated from healthy controls (HC) and rheumatoid arthritis (RA) patients, on naïve T cell differentiation. We demonstrated that CpG-induced B10 cells from HC drove naïve T cell differentiation toward regulatory T cells (Treg cells) and IL-10-producing T cells (Tr1) through IL-10 secretion and cellular contacts. B10 cells from HC did not decrease T helper 1 (Th1) nor and tumor necrosis factor α producing T cell (TNFα T cell) differentiation. We showed that in RA, B10 cells could also induce Treg cells and Tr1 from naïve T cells. Contrary to HC, B10 cells from RA patients increased naïve T cell conversion into Th1. Interestingly, PD-L2, a programmed death-1 (PD-1) ligand that inhibits PD-L1 and promotes Th1 differentiation, was overexpressed on RA B10 cells compared to HC B10 cells. Together, our findings showed that CpG-induced B10 cells may be used to increase Treg cells in patients with RA. However, CpG may not be the most adequate stimuli as CpG-induced B10 cells also increased inflammatory T cells in those patients.