Our data suggest that the immune regulatory feedback between CD24+CD38hi Breg cells and pDCs that is in place in healthy individuals is dysfunctional in SLE patients but that this feedback is normalized in patients who respond to rituximab. It is tempting to suggest that when sufficient CD24+CD38hi Breg cells have been generated at a site of inflammation by IFN-α+ pDCs or after CD40-CD40L interactions with T cells, for instance, Breg cells can then prevent pDCs from producing excessive IFN-α that would otherwise drive chronic inflammation. This evidence concerns the gene CD40 and systemic lupus erythematosus.