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Departments of
*
Rheumatology and
Allergy and Respiratory Diseases, Guy’s, King’s and St. Thomas School of Medicine, King’s College London, Guy’s Hospital, London, United Kingdom;
Protein Sequencing Laboratory, Imperial Cancer Research Fund, London, United Kingdom;
Department of Pediatrics, UT Medical Group Inc., Memphis, TN 38163;
¶ Department of Orthopedic Surgery, School of Medicine, Wayne State University, Hutzel Hospital, Detroit, MI 48201;
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Infection and Immunity Research Group, King’s College London, London, United Kingdom; and
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Institute of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands
Rheumatoid arthritis (RA) is the most common, crippling human autoimmune disease. Using Western blotting and tandem mass spectroscopy, we have identified the endoplasmic reticulum chaperone BiP, a 78-kDa glucose-regulated protein, as a possible autoantigen. It preferentially stimulated increased proliferation of synovial T cells from patients with RA but not from patients with other arthritides. Mice with established collagen- or pristane-induced arthritis developed IgG Abs to BiP. Although BiP injected in CFA failed to induce arthritis in several strains of rats and mice, including HLA-DR4+/-- and HLA-DR1+/+-transgenic animals, it completely inhibited the development of arthritis when given i.v. 1 wk before the injection of type II collagen arthritis. Preimmunization with BiP suppressed the development of adjuvant arthritis in Lewis rats in a similar manner. This is the first report of a mammalian chaperone that is an autoantigen in human RA and in experimental arthritis and that can also prevent the induction of experimental arthritis. These findings may stimulate the development of new immunotherapies for the treatment of RA.
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