Investigators at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) have identified a novel disease mechanism underlying rheumatoid arthritis that may open the door to new therapies for this and other debilitating autoimmune disorders.
In an article appearing in the September 1 issue of the Journal of Immunology, principal investigator Terry J. Smith, MD describes research that identifies an interaction between antibodies found in patients with rheumatoid arthritis and the insulin-like growth factor receptor (IGF-1R) as a cause of inflammation and lymphocyte infiltration. Dr.Smith published similar results last year dealing with Graves' disease, an autoimmune disorder affecting the thyroid gland and eyes.
Dr. Smith and his colleagues found that specific immunoglobins "turn on" the IGF-1R much like IGF-1 itself is known to do. Once the receptor is "on", a number of molecular events occur, including the production of two very powerful factors known to trigger T lymphocytes and direct them to sites of inflammation.
In addition, the researchers found that blocking the interaction between the antibodies and IGF-1R arrests the progression of molecular events leading to T cell activation.
According to Dr. Smith, "It is possible that these findings will allow us for the first time to interrupt the disease process before any lasting damage occurs."
Rheumatoid arthritis is one of several autoimmune disorders in which cellular defense mechanisms identify the body's own tissues as foreign and seek to destroy them. Other autoimmune disorders include such ailments as Graves' disease, multiple sclerosis and lupus. This research suggests that there could be a common therapeutic strategy for these conditions.
According to Kenneth P. Trevett, JD, President and CEO of LA BioMed, "The research by Dr. Smith offers the promise of a magic bullet treatment for several autoimmune diseases."