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    Antitopoisomerase I monoclonal autoantibodies from scleroderma patients and tight skin mouse interact with similar epitopes.

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    79
    Author
    Muryoi, T; Kasturi, KN; Kafina, MJ; Cram, DS; Harrison, LC; Sasaki, T; Bona, CA
    Date
    1992-04-01
    Source Title
    Journal of Experimental Medicine
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    Harrison, Leonard
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Muryoi, T., Kasturi, K. N., Kafina, M. J., Cram, D. S., Harrison, L. C., Sasaki, T. & Bona, C. A. (1992). Antitopoisomerase I monoclonal autoantibodies from scleroderma patients and tight skin mouse interact with similar epitopes.. J Exp Med, 175 (4), pp.1103-1109. https://doi.org/10.1084/jem.175.4.1103.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259350
    DOI
    10.1084/jem.175.4.1103
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119171
    Abstract
    We have generated for the first time monoclonal antibodies (mAbs) specific for topoisomerase I (topo I) from scleroderma patients, and tight skin mice which develop a scleroderma-like syndrome. The epitope specificity of these antibodies has been determined using a series of fusion proteins containing contiguous portions of topo I polypeptide. Western blot analysis demonstrated that both human and mouse mAbs bound strongly to fusion protein C encompassing the NH2-terminal portion of the enzyme, and weakly to fusion proteins F and G containing regions close to the COOH-terminal end of the molecule. This crossreactivity is related to a tripeptide sequence homology in F, G, and C fusion proteins. It is interesting that a pentapeptide sequence homologous to that in fusion protein C was identified in the UL70 protein of cytomegalovirus, suggesting that activation of autoreactive B cell clones by molecular mimicry is possible. Both human and mouse mAbs exhibiting the same antigen specificity, also share an interspecies cross-reactive idiotope. These data suggest that B cell clones producing antitopo autoantibodies present in human and mouse repertoire are conserved during phylogeny, and are activated during the development of scleroderma disease.

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