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Cerebral ischemia is accompanied by fulminant cellular and humoral inflammatory changes in the brain which contribute to lesion development after stroke.

A tight interplay between the brain and the peripheral immune system leads to a biphasic immune response to stroke consisting of an early activation of peripheral immune cells with massive production of proinflammatory cytokines followed by a systemic immunosuppression within days of cerebral ischemia

Recent work has documented the importance of T lymphocytes in the early exacerbation of ischemic injury.

We found that treatment with FTY720 (1mg/kg) reduced lesion size and improved neurological function after experimental stroke in mice,

The profound damage to the CNS caused by ischemic lesions has been well documented. Yet, relatively little is known about the contribution to and effects on the immune system during stroke.

These novel findings advocate the need to develop or effectively utilize agents that can block early neural splenic activation and modulate immune cells specific for brain antigens as a means to prevent mobilization of T and B cells carrying a cytokine death warrant to the brain.

HONG KONG, Aug 3 (Reuters) - Scientists have identified a class of immune cells that floods the brain soon after a stroke, causing inflammation and more neurological damage.

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," Yoshimura said.

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 said.

The experts hope to apply the findings of the study, published in Nature Medicine, on people.

He added that an experimental antibody against interleukin-23 is currently in phase 2 clinical trial.

"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," he added.