Genomic and proteomic studies in systematic Lupus Erythematosus pateints with distinct autoantibody specificities to nuclear autoantigens

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease with enormous heterogeneity in clinical manifestations and autoantibody repertoires. The classical manifestations of SLE include nephritis, pericarditis, arthritis, rashes, etc., and are supposed to result from exuberant autoantibody responses against nuclear and cytoplasmic components. Two major groups of autoantibodies present in SLE patients are predominantly directed against nuclear antigens specifically double stranded DNA (dsDNA) and extractable nuclear antigens (ENA) though, the mechanisms underlying this distinct autoantibody profile is poorly understood (Sherer et al., 2004; To et al., 2005). The etiology of SLE is multifactorial involving genetic, environmental and epigenetic factors (Hocheberg et al., 1997; Danchenko et al., 2006). However, there is no general unifying theory which could explain the basis of heterogeneity in autoantibody repertoire.