The vicious pathogenic spiral responsible for the autoimmune process in SLE, likely mediated by the sustained secretion of type I IFN [15], is thought to occur as follows: pDC-derived type I IFN rapidly triggers the differentiation and activation of myeloid DCs, which in turn elicits the differentiation of autoreactive CD4+ T cells, CD8+ T cells, and B cells as antigen-presenting cells through processing self-components. Here, CD8A is linked to systemic lupus erythematosus.