Advertisement
Research Article Free access | 10.1172/JCI105669
Department of Medicine, New York University School of Medicine, New York
Department of Biochemistry, Tufts University School of Medicine, Boston, Massachusetts
‡Clinical Scholar, The Arthritis Foundation.
Address requests for reprints to Dr. Naomi Rothfield, New York University Medical Center, School of Medicine, Department of Medicine, 550 First Avenue, New York, N. Y. 10016.
*Received for publication 2 May 1967 and in revised form 14 July 1967.
Presented in part at a joint meeting of the American Society for Clinical Investigation and the American Federation for Clinical Research on 30 April 1967 in Atlantic City, N. J.
This study was supported by grants from the National Institute of Allergy and Infectious Diseases (AI 06853), the Lupus Foundation, and the National Science Foundation (GB 5606).
Find articles by Rothfield, N. in: JCI | PubMed | Google Scholar
Department of Medicine, New York University School of Medicine, New York
Department of Biochemistry, Tufts University School of Medicine, Boston, Massachusetts
‡Clinical Scholar, The Arthritis Foundation.
Address requests for reprints to Dr. Naomi Rothfield, New York University Medical Center, School of Medicine, Department of Medicine, 550 First Avenue, New York, N. Y. 10016.
*Received for publication 2 May 1967 and in revised form 14 July 1967.
Presented in part at a joint meeting of the American Society for Clinical Investigation and the American Federation for Clinical Research on 30 April 1967 in Atlantic City, N. J.
This study was supported by grants from the National Institute of Allergy and Infectious Diseases (AI 06853), the Lupus Foundation, and the National Science Foundation (GB 5606).
Find articles by Stollar, B. in: JCI | PubMed | Google Scholar
Published November 1, 1967 - More info
Sera from 55 patients with systemic lupus erythematosus were studied to clarify the significance of the patterns of nuclear fluorescence observed. The sera in which the IgG fraction produced a peripheral pattern of nuclear fluorescence were found to contain complement-fixing antibodies to native DNA and to DNA-histone complexes. This correlation did not exist when complement-fixing activity was compared to the IgM nuclear patterns. Sera which contained only complement-fixing antibodies to denatured DNA and which did not react with native DNA or nucleoprotein did not produce the peripheral pattern of nuclear fluorescence. The data suggest that single strands of DNA were not the reactive groups in the nucleus responsible for the peripheral pattern. The results support the conclusion that DNA within a DNA-protein complex may be the nuclear antigen responsible for the peripheral pattern of nuclear fluorescence.
Analysis of the clinical data revealed that a close correlation existed between the presence of IgG peripheral pattern, complement-fixing antibodies to DNA and histone-DNA complexes, and clinical manifestation of active disease.
Images.