Rheumatoid arthritis is one of the most common autoimmune diseases. It occurs when immune cells called T cells accumulate in the joints and attack the body's own tissue, causing painful swelling. Now researchers may have gained an important insight into what makes the T cells pile up.
Researchers already knew that T cell migration is triggered by chemical messengers called chemokines. Chemokines are produced by a variety of cell types, including connective tissue cells called fibroblasts. What prompts the fibroblasts to produce abnormally high levels of chemokines in people with rheumatoid arthritis isn't known. However, 2 years ago, Terry Smith of the Harbor-University of California, Los Angeles, Medical Center in Torrance and colleagues discovered that in patients with Graves disease--an autoimmune disorder that attacks the thyroid gland and eyes--fibroblasts make chemokines when so-called immunoglobulin G antibodies in the blood activate a protein called the insulin-like growth factor 1 (IGF-1) receptor. To see if the same chain of events happens in rheumatoid arthritis, Smith's team tested whether various kinds of fibroblasts would spur T cell migration in test tubes.
Nothing happened--until immunoglobulin G antibodies were added to the test tube, the team found. The T cell migration halted again when the team added a chemical that blocks the IGF-1 receptor, the authors report 23 August in the Journal of Immunology. They also found that antibodies from Graves patients activated IGF-1 receptors in fibroblasts from rheumatoid arthritis patients (and vice versa), triggering chemokine production and T cell migration. That suggests that IGF-1 receptors may be key players in multiple autoimmune disorders. Moreover, the receptor could be an attractive therapeutic target for both rheumatoid arthritis and Graves disease, says Smith.
Rheumatologist Thomas Pap of the University Hospital Magdeburg in Germany agrees that the research could lead to "innovative therapeutic strategies." He says that the findings "add a completely new aspect" to the role of antibodies in autoimmune diseases.
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