An increase in the maturation phenotype of DCs, such as upregulated expression of co-stimulatory molecules, such as CD86, and increased secretion of pro-inflammatory cytokines, such as IL-12 and IFN-I, have been documented in systemic lupus erythematosus (SLE) patients [201, 202]. This evidence concerns the gene CD86 and systemic lupus erythematosus.