Different factors contribute to the development of spontaneous GC and enhanced risk of developing autoimmunity in humans and mice, such as BAFF (30, 31) and IFNγ−receptor (32, 33) overexpression, inflammatory cytokines, constitutive CD40 signaling (34), and human endogenous retrovirus (HERV) expression (35), etc. PRL could act as one of these factors, since our results also showed a positive correlation between PRL levels and absolute numbers of B-GCs in the spleen, and in vitro differentiation of FO B cells showed preferential formation of B-GCs. This evidence concerns the gene TNFSF13B and Autoimmunity.