A large number of studies have indicated that cytokines such as IFN and ILs derived from pDCs and T cells, the expression of CD19 and BCR, and the interaction of transporters such as UNC93B1 and SLC15A4 with TLRs operate in a complex network that controls autoreactive antibody responses to nucleic acid antigens and results in the complex pathogenesis and symptom heterogeneity of SLE. Here, CD19 is linked to systemic lupus erythematosus.