Immune cells cause post-stroke damage

It has been almost 5 years since this came out. If we had anything resembling a decent stroke association a solution to this problem would have been found and disseminated.
http://www.abc.net.au/science/articles/2009/08/03/2644218.htm

Scientists have identified a class of immune cells that floods the brain soon after a stroke, causing inflammation and more neurological damage.

In an experiment, Japanese researchers showed how mice that were deficient in these immune cells suffered far less brain damage after a stroke compared to normal mice.
The lead author of the study, Akihiko Yoshimura at Keio University's School of Medicine in Tokyo, says that while the initial damage from a stroke cannot be prevented, drugs can be used to limit secondary damage caused by immune cells that rush to the site of the infarction, or stroke.
"The first damage happens immediately after a stroke, we can't block this because it is very rapid," says Yoshimura.
"But after this neural damage, macrophages and T-cells (two types of immune cells) are imported and this inflammation induces the growth of the infarction. We can block this secondary damage by suppressing the inflammation," he says.

Turning on itself

The body's natural defence system produces immune cells to fight off invading viruses and bacteria, and in the event of any injury. Unfortunately, the same mechanism kicks in after a stroke-induced injury.
In their experiment, Yoshimura and his colleagues induced a stroke in several groups of mice and observed how the subsequent flood of immune cells caused inflammation and more damage.
One of the first groups of immune cells to enter the brain is called interleukin-23 (IL-23).
"IL-23 itself is not harmful, but it activates other immune cells like T-cells and macrophages and these attack the brain. This same sort of activation occurs when the body is invaded by microbes and during any sort of injury," says Yoshimura.
The mice that suffered the least brain damage were those genetically engineered to be deficient in IL-23.
"IL-23 operates immediately after stroke or one day later ... so the sooner the intervention (blocking of IL-23) happens, the more protective it is for the brain," he says.

Treatment

The experts hope to apply the findings of the study, published in Nature Medicine, on people.
"Most patients come to hospital within a day after a stroke, so we need to develop a therapeutic method to prevent the expansion of infarction," says Yoshimura.
"Our study is important because it provides a therapeutic target. We should start to treat patients one day after stroke happens (to block the infiltration of immune cells)."
Yoshimura adds that an experimental antibody against interleukin-23 is currently in phase 2 clinical trial. (Where are the results?)
"It is to be used for inflammatory diseases, like inflammatory bowel disease. So if it is approved, we can try this drug on stroke patients.'