The course of a stroke was previously described by scientists as follows: A blood vessel supplying the brain with oxygen and vital nutrients is suddenly blocked by a blood clot. This leads to a stroke, causing injury to the brain. As a result, many patients suffer from neurological dysfunctions, such as severe paralysis or speech disorders.
"This picture must be supplemented by another important factor, namely the immune system," says Professor Christoph Kleinschnitz, head of stroke medicine at the University of Würzburg's Department of Neurology. He verified this in a joint project with the study group of Professor Heinz Wiendl at the University Hospital of Münster.
The new insight was discovered in mice the immune system of which lacks regulatory T cells due to a genetic defect: The brain damage sustained by these mice after a stroke is reduced by about 75 percent as compared to normal mice. Furthermore, these mice develop significantly fewer neurological dysfunctions.
Regulatory T helper cells are an important part of the immune system and usually have the task of suppressing excessive immune responses of the body. Due to their regulatory properties, they play a protective role in many diseases, such as multiple sclerosis or rheumatism.
"The fact that regulatory T cells aggravate the brain damage to this extent in acute stroke cases came as a complete surprise to us," reports Wiendl. "We can say without exaggeration that this constitutes a paradigm shift from the perspective of immunology."
In their research, the immunologists also investigated with which mechanisms the regulatory T cells exacerbate the harmful effect of a stroke. They found out that this cell type interacts with platelets and blood vessel walls, especially in the early stages after a stroke. This worsens the clotting of the cerebral vessels, further reducing the cerebral blood flow.
The scientists are now going to determine whether the results can be applied to humans. Should this be the case, strokes might be treated in future with drugs that affect regulatory T cells.
MEDICA.de; Source: University of Würzburg