Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology (1–4). Clinical features of SLE include fatigue, fever, dermatitis, photosensitivity, alopecia, arthritis, serositis, hematologic abnormalities, mucosal ulcerations, Raynaud’s phenomenon, neurological disease, and glomerulonephritis. Serologic features include false positive VDRL, antibodies to nuclear constituents, leukocytes, and erythrocytes, circulating immune complexes, and depressed complement levels. Although genetic (5), hormonal (6), and environmental (7) factors have been implicated in the etiology and modification of disease activity, immunologic abnormalities are postulated as essential in the pathogenesis of disease (8, 9). Polyclonal B cell hyperactivity with formation of large amounts of autoantibodies is characteristic of SLE (10–12). A number of effector and regulatory T cell defects have also been described (13–15). However, the clinical manifestations of disease appear to be secondary to the inflammatory response initiated by immune complexes (16,17). DNA-anti-DNA complexes may be of especial pathogeneic importance (18–20).
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Huston, D.P. (1984). Systemic Lupus Erythematosus. In: Suki, W.N., Massry, S.G. (eds) Therapy of Renal Diseases and Related Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3807-9_19
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DOI: https://doi.org/10.1007/978-1-4613-3807-9_19
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