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Autoantibodies to topoisomerase I in a patient with systemic lupus erythematosus without features of scleroderma

Departments of Medicine and Microbiology/Immunology, Thurston Arthritis Research Center and UNC Lineberger Comprehensive Cancer Center, University of North Carolina, 3330 Thurston Building, CB no. 7280, Chapel Hill, NC 27599-7280

M. Satoh

Departments of Medicine and Microbiology/Immunology, Thurston Arthritis Research Center and UNC Lineberger Comprehensive Cancer Center, University of North Carolina, 3330 Thurston Building, CB no. 7280, Chapel Hill, NC 27599-7280

M.A. Dooley

Departments of Medicine and Microbiology/Immunology, Thurston Arthritis Research Center and UNC Lineberger Comprehensive Cancer Center, University of North Carolina, 3330 Thurston Building, CB no. 7280, Chapel Hill, NC 27599-7280

M. Kuwana

Division of Rheumatology and Clinical Immunology, Department of Internal Medicine, University of Pittsburgh, Pittsburgh, PA

J.C. Jennette

Department of Pathology, University of North Carolina, Chapel Hill, NC 27599, USA

W.H. Reeves

Departments of Medicine and Microbiology/Immunology, Thurston Arthritis Research Center and UNC Lineberger Comprehensive Cancer Center, University of North Carolina, 3330 Thurston Building, CB no. 7280, Chapel Hill, NC 27599-7280

We report a woman with systemic lupus erythematosus (SLE) with diffuse proliferative glomerulonephritis and anti-dsDNA antibodies whose serum contained autoantibodies specific for the phosphorylated form of RNA polymerase II (RNAP IIO), Su and ribosomal P antigen, as well as anti-topoisomerase I antibodies, a marker for scleroderma (SSc). Over 6 years, the patient exhibited clinical manifestations consistent with SLE without clinical evidence of scleroderma. The reactivity of her serum autoantibodies with the phosphoproteins ribosomal P, topoisomerase I, and RNAP IIO is consistent with recognition of autoepitopes comprised in part of phosphate groups. This may explain the unexpected coexistence of marker autoantibodies for SLE and scleroderma, possibly with implications for the mechanisms of autoantibody generation.

Key Words: anti-topoisomerase I antibodies • anti-RNA polymerase II antibodies • anti-nuclear antibodies

Lupus, Vol. 4, No. 4, 314-317 (1995)
DOI: 10.1177/096120339500400414


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