Immune System Breakthrough May Benefit Rheumatoid Arthritis
Posted Jan 17 2011 5:47pm
Rheumatoid arthritis (RA) is an autoimmune disease that causes the body’s immune system to attack itself. Many treatments have been investigated that would control or suppress the body’s immune system. Anti tumor necrosis factor (TNF) drugs are immune system suppressants that are widely used to treat RA.
A new study conducted by researchers at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge has resulted in a breakthrough in the understanding of how autoimmune responses can be controlled.
In a normal immune system, the body develops immune cells to recognize foreign material, like bacteria. Once encountered, the immune cells respond to eliminate the foreign material. Any rogue immune cells that would attack the body itself are destroyed during development or are regulated by special cell. A key gene in these regulatory cells is called Foxp3. Those people that either lack the Foxp3 gene or have a mutated version of the gene have dysfunctional immune regulation which can result in autoimmune diseases.
As a part of the study, scientists created a genetically engineered form of Foxp3 that can change developing immune cells into regulatory cells that have the ability to suppress immune response. They then injected the engineered gene into animals that were missing the Foxp3 gene.
Said group leader Dr. Alexander Betz: “When administered to and activated in animal models of arthritis, the modified cells inhibit or even reverse the disease process.”
The scientists are now working on determining the molecular mechanisms involved in the functioning of the Foxp3 gene and applying that to human cells. In that research they need to ensure that the human form of the gene does not negatively impact the body’s immune system.
“If Foxp3 functions as a key developmental switch in human immune cells, there is potential for a new avenue of therapy development that could transform arthritis treatment” — Dr. Betz.
The study was published in the current issue of the journal PLoS Biology.