Cambridge: Type 1 diabetes, lupus and rheumatoid arthritis are autoimmune diseases, which are a result of the inadequacy of the immune system// to check itself.
Researchers are still unsure about the location of the molecular breakdowns, which are responsible for weakening the immune system. Now, a team of scientists from the Whitehead Institute and the Dana-Farber Cancer Institute have discovered a crucial group of genes which form the heart of autoimmune disease.
"This may shorten the path to new therapies for autoimmune disease," says Whitehead Member and MIT professor of biology Richard Young, senior author on the paper that will appear January 21 online in Nature. "With this new list of genes, we can now look for possible therapies with far greater precision."
The immune system is often described as a kind of military unit, a defense network that guards the body from invaders. Seen in this way, 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.
Scientists previously discovered that 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 aPage: 1 2 Related medicine news :1
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