Autoimmune Diseases Share Inflammatory Mechanism

Researchers have found that antibodies from patients with rheumatoid arthritis are able to induce cytokine production through the insulin-like growth factor-1 receptor (IGF-1R) pathway in a fashion identical to that previously shown for antibodies from patients with Grave's disease.

Investigators from the University of California, Los Angeles (USA), reported in the September 1, 2004, issue of the Journal of Immunology that antibodies from individuals with active rheumatoid arthritis (RA-IgG) stimulate their synovial fibroblasts to express the CD4-specific T lymphocyte chemoattractant, IL-16, and RANTES, a C-C chemokine. This induction, which is identical to that previously reported for patients with Grave's disease, is mediated through the insulin-like growth factor-1 receptor (IGF-1R) pathway. Antibodies from individuals without known autoimmune disease fail to elicit this chemoattractant production.

If these findings can be extended to other autoimmune disorders such as multiple sclerosis and lupus, it may be possible to develop a common therapeutic strategy for these conditions. Senior author Dr. Terry J. Smith, a professor in the division of molecular medicine at UCLA said, "It is possible that these findings will allow us for the first time to interrupt the disease process before any lasting damage occurs.”




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