cell alterations in this disease is not known here we demonstrate that sle serum induced monocyte derived dcs sle dcs can efficiently stimulate na u00efve and memory b cell differentiation into igg and iga plasmablasts pbs phenotypically identical to those found expanded in the blood of sle patients sle dc mediated igg pb differentiation is dependent on b cell activating factor baff and il 10 in contrast iga pb differentiation is dependent on a proliferation inducing ligand april but not baff nor il 10 more importantly sle dcs upregulate the expression of cd138 and trans present april to b cells which is the key mechanism responsible for the sle dc mediated iga responses this feature of sle dcs is not shared by dcs generated with ifn u03b1 ifn dcs and thus ifn dcs are much less efficient at inducing iga responses in addition sle dcs induce the expression of bcl x l in pbs and support their survival further enhancing igg and iga responses thus our study supports that a direct interplay between dcs and b cells might contribute to enhance pathogenic antibody responses in sle however the mechanisms underlying the failure to maintain b cell tolerance in sle remain incompletely characterized there are multiple checkpoints during b cell development maturation and activation that have been demonstrated to be defective in murine lupus models grimaldi et al 2002 grimaldi et al 2001 kuo et al 1999 santulli marotto et al 2001 as well as in sle patients wardemann et al 2003 yurasov et al 2006 yurasov et al 2005.