Patients with systemic rheumatic diseases such as systemic lupus erythematosus (SLE), scleroderma, and Sjogren's syndrome characteristically produce antinuclear antibodies (ANAs) that recognize intracellular nucleoprotein complexes. Systemic rheumatic diseases constitute chronic, life-threatening, multiorgan autoimmune disorders (Reichlin 1998). Their etiology is unknown, but genetic, hormonal, and environmental factors are involved. SLE is best characterized as a systemic immune complex vasculitis due to continued production of autoantibodies directed against nucleoplasmic antigens (e.g., DNA, histones, spliceosomal components, ribonucleo-proteins), whereas scleroderma-associated autoantibodies primarily detect nucleo-lus-associated proteins such as DNA topoisomerase I (Scl-70) and centromeres. Autoantibodies target evolutionary, conserved epitopes of nucleoprotein complexes, which often constitute the functional regions (Tan 1989). Thus, the immunofluores-cence staining patterns observed with autoantibody-containing serum samples can be regarded as an autoantigenic map that provides information on the subcellular distribution and function of the target antigens (Hemmerich and von Mikecz 2000, Tan 1991). Humoral autoimmune responses seem to be antigen driven and T-cell dependent (Lanzavecchia 1995). However, the molecular mechanisms responsible for stimulating autoreactive B and T cells, as well as for the generation of a systemic autoimmune response against the cell nucleus, remain unclear and represent an intensively investigated topic of current immunology.
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