We demonstrated that bone marrow cells differentiated with GM-CSF for 7 days in the presence of RA had an activated regulatory phenotype (i.e. increased CD80, CD86, MHC class II, PD-L1 and PD-L2), produced increased IL-10, increased the induction of Treg and suppressed the proliferation of responder immune cells. This evidence concerns the gene CSF2 and rheumatoid arthritis.