Foxp3

This schematic represents the researchers' strategy to identify where Foxp3 physically interacts with the genome in T cells. The background is a microarray where the red probes reveal regions of DNA where Foxp3 is bound.
(Image: Tom DiCesare)
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The immune system is a defense network that guards the body from invaders.
Autoimmune diseases such as type 1 diabetes, lupus and rheumatoid arthritis occur when the immune system fails to regulate itself. But researchers have not known precisely where the molecular breakdowns responsible for such failures occur.

Now, a team of scientists from the Whitehead Institute and the Dana-Farber Cancer Institute have identified a key set of genes that lie at the core of autoimmune disease, findings that may help scientists develop new methods for manipulating immune system activity.

A group of white blood cells called T cells are the frontline soldiers of immune defense, engaging invading pathogens head on. These T cells are commanded by a second group of cells called regulatory T cells. Regulatory T cells prevent biological "friendly fire" by ensuring that the T cells do not attack the body's own tissues. Failure of the regulatory T cells to control the frontline fighters leads to autoimmune disease.

Regulatory T cells are themselves controlled by a master gene regulator called Foxp3. Master gene regulators bind to specific genes and control their level of activity, which in turn affects the behavior of cells.

In fact, when Foxp3 stops functioning, the body can no longer produce working regulatory T cells. When this happens, the frontline T cells damage multiple organs and cause symptoms of type 1 diabetes and Crohn's disease. However, until now, scientists have barely understood how Foxp3 controls regulatory T cells because they knew almost nothing about the actual genes under Foxp3's purview.

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