FOXP3 and systemic lupus erythematosus: Together, these data reveal that the increased frequency of FOXP3+ Tregs observed in SLE patients is not caused by a selective expansion of non-conventional or peripherally induced Tregs, which could be less functional or even promoting the production of pro-inflammatory cytokines, but rather by the expansion of bona-fide thymically-derived FOXP3+HELIOS+ Tregs, showing the hallmarks of suppressive functions.