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Research Article Free access | 10.1172/JCI114199

Role of antigen selectivity in autoimmune responses to the Ku (p70/p80) antigen.

W H Reeves, Z M Sthoeger, and R G Lahita

Rockefeller University, New York 10021.

Find articles by Reeves, W. in: PubMed | Google Scholar

Rockefeller University, New York 10021.

Find articles by Sthoeger, Z. in: PubMed | Google Scholar

Rockefeller University, New York 10021.

Find articles by Lahita, R. in: PubMed | Google Scholar

Published August 1, 1989 - More info

Published in Volume 84, Issue 2 on August 1, 1989
J Clin Invest. 1989;84(2):562–567. https://doi.org/10.1172/JCI114199.
© 1989 The American Society for Clinical Investigation
Published August 1, 1989 - Version history
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Abstract

Levels of anti-Ku (p70/p80) antibodies were measured longitudinally in sera from four individuals with systemic lupus erythematosus or related disorders. Antibodies to the native Ku antigen (p70/p80 complex) varied over a range of up to 577-fold. Large fluctuations were also observed in the levels of autoantibodies to several distinct epitopes of the Ku (p70/p80) antigen. Levels of these individual autoantibody populations generally paralleled one another, suggesting that they are coordinately regulated. A similar pattern of anti-DNA antibody fluctuation was seen in some sera. To examine the possibility that these autoantibodies were generated by polyclonal B cell activation, the levels of anti-Ku (p70/p80) and anti-DNA antibodies were compared to the levels of antibodies to Escherichia coli proteins, tetanus toxoid, and bovine insulin, transferrin, cytochrome c, serum albumin, and thyroglobulin. In sera from the same individual, anti-Ku (p70/p80) antibodies were sometimes produced in the complete absence of polyclonal activation, and at other times were accompanied by increased polyclonal activation. Anti-DNA antibody levels more closely paralleled the level of polyclonal activation than did the anti-Ku (p70/p80) levels. These studies suggest that anti-Ku (p70/p80) antibodies are generated by an antigen-selective mechanism, but that polyclonal activation frequently, although not invariably, accompanies autoantibody production. This observation is consistent with the possibility that polyclonal activation might be secondary to autoantibody production.

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