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T-cell suicide stops mice fighting off flu

More bad press for free radicals. Now it seems that too many of them can impair the mouse immune system, making them unable to fight off flu.

The finding could shed light on the cause of many mysterious human immunodeficiency disorders, such as severe combined immunodeficiency (SCID), says Frederick Domann at the University of Iowa, Iowa city.

Free radicals are natural by-products of metabolism, which bind to molecules, including proteins and DNA. But oxidative damage is linked to many diseases such as lung cancer, atherosclerosis and Alzheimer's.

However, no one knew if free radicals also affected an important arm of the immune system which uses T-cells. A type of white blood cell, T-cells are supposed to attack invaders but they can also malfunction, leading to autoimmune disorders.

Domann and colleagues created mice with elevated levels of a free radical called superoxide by knocking out the gene SOD2, which normally mops up superoxide.

Elevated levels of superoxide had "severe effects on T-cell development," says Domann.

Normally, when T-cells are no longer working properly they self-destruct in a process called apoptosis. This is to prevent them attacking the body's own cells.

According to Domann, excess free radicals appear to alter the signalling process responsible for apoptosis, prompting functional T-cells to suicide unnecessarily. "Superoxide makes these cells die in very high numbers," he says.
 
 

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