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Author Notes:

The authors thank Kim Turley and Rana Muneer for excellent technical assistance and Mary Patterson and Cricket Baughman for typing the manuscript. We also thank Drs. Edwin H. Beachey and Vincent A. Fischetti for sharing with us preparations from their laboratories and for their encouragement throughout the project. We also thank Dr. Joseph J. Ferretti for his support and encouragement and for his critical review of this manuscript.

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Research Funding:

This work was supported by grant 841337 from the American Heart Association (AHA), funded in part by the AHA, Oklahoma Affiliate.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Immunology
  • Research & Experimental Medicine

Polyspecificity of antistreptococcal murine monoclonal antibodies and their implications in autoimmunity

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Journal Title:

Journal of Experimental Medicine

Volume:

Volume 164, Number 4

Publisher:

, Pages 998-1012

Type of Work:

Article | Final Publisher PDF

Abstract:

mAbs produced by immunization of BALB/c mice with Streptococcus pyogenes M type 5 membranes were further characterized for their reaction with S. pyogenes pep M5 protein and with autoantigens associated with human cell lines. mAbs 36.2.2 and 54.2.8 simultaneously reacted with M protein and a membrane protein(s) of S. pyogenes. When cell lines were mixed with 54.2.8, we saw nuclear fluorescence along with staining of the cytoskeleton. Subsequent experiements revealed that 54.2.8 was an anti-DNA antibody that reacted with DNA, poly(I), poly(dT), and weakly with cardiolipin. Its reactivity with the cytoskeleton could be blocked with anti-vimentin. On the other hand, 36.2.2 reacted with the cytoskeleton, sparing the nucleus, and was inhibited by the α helical proteins myosin, actin, and keratin. mAb 54.2.8 was inhibited with myosin, but not with actin and keratin. None of the antibodies studied were inhibited by collagen, and none of them were rheumatoid factors. The results imply that Group A stretococci activate B cell clones against myosin, α helical proteins, or DNA, thereby contributing to the enhancement of autoantibody production.

Copyright information:

© The Rockefeller University Press.

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