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Systemic lupus erythematosus (SLE) is a generalized autoimmune disease affecting several organ systems, characterized by the presence of a vast array of autoantibodies, characteristically directed to nuclear antigens (ANA) (Arbuckle et al, 2003, Hahn, 1998, Rothman and Isenberg, 2008). Systemic lupus erythematosus (SLE) is the second most common human autoimmune disease affecting between 400 and 1000 per million people worldwide (Craft, 2011). SLE is caused by the breakdown of tolerance to nuclear self-antigens, which leads to activation of autoreactive B cells that produce autoantibodies against self-nucleic acids and associated proteins (Lande et al, 2011). These autoantibodies bind self-nucleic acids released by dying cells, and form immune complexes that are deposited in different parts of the body, leading to detrimental inflammation and tissue damage. A key early event that triggers autoimmunity in SLE is the chronic innate activation of plasmacytoid dendritic cells (pDCs) to secrete type I interferons (IFNs) (Theofilopoulos et al, 2005; Ronnblom et al, 2006; Banchereau and Pascual, 2006). The high levels of type I IFNs induce an unabated differentiation of monocytes into dendritic cells that stimulate autoreactive B and T cells (Blanco et al, 2001), licensing T cells recognize autoantigens and lower the activation threshold of autoreactive B cells (LeBon et al, 2006), thereby promoting autoimmunity in SLE. Analysis of genes encoding components of the interferon pathway has led to extensive support for an association of polymorphic variants of interferon regulatory factor 5 (IRF5) with SLE (Bennett et al, 2003; Crow, 2008; Niewold et al,2007;). Recent genomewide association studies confirm associations of HLA and STAT4 variants with SLE and also the role of PTPN22 (International Consortium, 2008; Rieck et al, 2007; Remmers et al, 2007). New reports of genetic SNPs associations include the B-cell-receptor–signaling pathway and the mechanisms of adhesion of inflammatory cells to the vasculature (Hom et al, 2008; Kozyrev et al, 2008). The heterogeneity of clinical manifestations and the disease's unpredictable course (Tan et al, 1982) characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and production

Fas Pathway of Cell Death and B Cell Dysregulation in SLE