IL-10 Producing B Cells Ability to Induce Regulatory T Cells Is Maintained in Rheumatoid Arthritis

Despite growing evidence highlighting the relevance of increasing I L-10-producing B cells (B10(+)cells) 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 (IRA) patients, on naive T cell differentiation. We demonstrated that CpG-induced B10(+) cells from HC drove naive 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 alpha producing T cell (TNF alpha(+) T cell) differentiation. We showed that in RA, B10(+) cells could also induce Treg cells and Tr1 from naive T cells. Contrary to HC, B10(+) cells from RA patients increased naive 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.