Prolactin Rescues Immature B-Cells from Apoptosis Induced by B-Cell Receptor Cross-Linking

Prolactin has an immunomodulatory effect and has been associated with b-cell-triggered autoimmune diseases,such as systemic lupus erythematosus (sle). in mice that develop sle,the prl receptor is expressed in early bone marrow b-cells,and increased levels of prl hasten disease manifestations,which are correlated with a reduction in the absolute number of immature b-cells. the aim of this work was to determine the effect of prl in an in vitro system of b-cell tolerance using wehi-231 cells and immature b-cells from lupus prone mrl/lpr mice. wehi-231 cells express the long isoform of the prl receptor,and prl rescued the cells from cell death by decreasing the apoptosis induced by the cross-linking of the b-cell antigen receptor (bcr) as measured by annexin v and active caspase-3. this decrease in apoptosis may have been due to the prl and receptor interaction,which increased the relative expression of antiapoptotic bcl-xl and decreased the relative expression of proapoptotic bad. in immature b-cells from mrl/lpr mice,prl increased the viability and decreased the apoptosis induced by the cross-linking of bcr,which may favor the maturation of self-reactive b-cells and contribute to the onset of disease. � 2016 rocio flores-fern�ndez et al.