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Myositis autoantibody inhibits histidyl-tRNA synthetase: a model for autoimmunity

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Abstract

In autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus (SLE), autoantibodies are generated against a variety of macromolecules. Myositis is a human autoimmune disease characterized by weakness and wasting of muscle1. In American studies2,3, antibodies directed against soluble cellular constituents were detected by immunodiffusion in about 60% of cases; the commonest of these, found in 25% of patients, was antibody to the Jo-1 antigen. An antibody system referred to as PL-1 was recognized at a similar frequency in a series of patients studied at Hammersmith Hospital, London4. We show here that this system is identical with the Jo-1 system and demonstrate that the antigen is a polypeptide of molecular weight (Mr) 50,000. The protein is immunoprecipitated with tRNAHis and appears to be histidyl-tRNA synthetase. The identity of the Jo-1 antigen, the first of the RNA-associated antigens familiar in autoimmune disease5,6 to be characterized as a specific enzyme, suggests a model for virus involvement in autoantibody generation.

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Authors and Affiliations

  1. Cold Spring Harbor Laboratory, PO Box 100, Cold Spring Harbor, New York, 11724, USA

    Michael B. Mathews

  2. Royal Postgraduate Medical School, Hammersmith Hospital, Ducane Road, London, W12 0HS, UK

    Robert M. Bernstein

Authors
  1. Michael B. Mathews
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  2. Robert M. Bernstein
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Mathews, M., Bernstein, R. Myositis autoantibody inhibits histidyl-tRNA synthetase: a model for autoimmunity. Nature 304, 177–179 (1983). https://doi.org/10.1038/304177a0

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  • DOI: https://doi.org/10.1038/304177a0

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