Numerous cellular and molecular abnormalities in immune cells, including T and B lymphocytes, monocytes, and dendritic cells (DCs), have been linked to the pathogenesis of SLE. SLE isa prototypicautoimmunedisease that can affect almost every organ of the human body. Factors that cause or contribute to disease range from endogenous genetic polymorphisms to environmental and infectious agents, all of which result in a severely dysregulated immune system [1–3]. The strong influence of genetic predispositions can be observed from the detection of mutations in single genes that are linked to the development of lupus-like symptoms in an array of disorders: mutations within 3′-repair DNA exonuclease 1 (TREX1), sterile α motif domain and HD domain-containing protein 1 (SAMDH1), and RNase H2 genes, among others. Rare gene deficiencies, including those of complement factors C1q, C2, and C4, result in lupus-like disorders, and aberrant splicing patterns [e.g., of the interferon-regulatory factor (IRF)-5 gene] have been linked to the development of SLE [4–7]. Of the genetic susceptibility regions identified, many relate to alleles that are well-established contributors to immune cell pathways, such as IRF-5 or tumor
