Current data suggest that abnormal APCs functions may be involved in the pathogenesis of SLE because the unusual functions of APCs may downregulate the expression of PD-L1 on their cell surface and result in failed antagonization of T cell signaling transduction mediated by CD80/CD86 and overactivation of effector T cells, thereby leading to lupus onset [93]. This evidence concerns the gene CD86 and systemic lupus erythematosus.