| Rheumatoid arthritis is a painful, inflammatory type of arthritis that occurs when the body's immune system attacks itself. A new paper, published in this week's issue of PLoS Biology, reports a breakthrough in the understanding of how autoimmune responses can be controlled, offering a promising new strategy for therapy development for rheumatoid arthritis. Normally, immune cells develop to recognise foreign material - antigens; including bacteria - so that they can activate a response against them. Immune cells that would respond to 'self' and therefore attack the body's own cells are usually destroyed during development. If any persist, they are held in check by special regulatory cells that provide a sort of autoimmune checkpoint. A key player in these regulatory cells is a molecule called Foxp3. People who lack or have mutated versions of the Foxp3 gene lack or have dysfunctional immune regulation, which causes dramatic autoimmune disease. Scientists at the Medical Research Council's Laboratory of Molecular Biology in Cambridge, and funded by the Arthritis Research Campaign, have genetically engineered a drug-inducible form of Foxp3. Using this, scientists can 'switch' developing immune cells into regulatory cells that are then capable of suppressing the immune response. Dr. Alexander Betz, Group Leader at the MRC laboratory, explains: "We have generated a modified form of Foxp3 which can be introduced into immune cells using genetic engineering techniques and then activated by a simple injection. When administered to and activated in animal models of arthritis, the modified cells inhibit or even reverse the disease process."
|