New understanding about how to control autoimmune responses offers promise in efforts to develop treatments for rheumatoid arthritis (RA), British researchers say.
RA -- a painful, inflammatory form of arthritis -- occurs when the body's immune system attacks itself. A molecule called Foxp3 plays an important role in immune system regulation. People who lack or have mutated versions of the Foxp3 gene lack or have dysfunctional immune system regulation.
Scientists at the Medical Research Council's Laboratory of Molecular Biology in Cambridge genetically engineered a drug-inducible form of Foxp3, which enables them to switch developing immune cells into regulatory cells capable of suppressing immune response.
The study was published in the current issue of the journal PLoS Biology.
"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," group leader Dr. Alexander Betz said in a PLoS Biology news release.
The researchers are now focusing on the molecular mechanisms involved in Foxp3 function and will then start working with human cells.
"First, we will develop a human Foxp3 factor and then assess its function in human arthritis models. To be viable as a therapeutic option, the regulatory cells must fulfill certain criteria: They must be tissue matched to the patient for compatibility; they must only block the targeted disease and not the whole body immune response; and they have to home correctly to their target tissue. Establishing these criteria will be the key focus of our research," Betz said.
"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," he added.
More information
The Arthritis Foundation has more about rheumatoid arthritis.
SOURCE: PLoS Biology, news release, Nov. 6, 2008
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