Immune responses and stroke brain damage - Anna Planas, IDIBAPS
Lack of oxygen and glucose supply to the brain causes rapid neuronal necrosis that releases danger signals. These signals induce innate immune responses triggering inflammation. Typical innate responses such as activation of the complement system and danger signal receptors are recognized to contribute to stroke brain damage. These signals activate resident glial cells and induce infiltration of circulating leukocytes. I will briefly present some of our work in this direction. Besides infiltration of myeloid cells, we now know that T cells also reach the brain very quickly after stroke, and several lines of evidence suggest that they can play a deleterious role.
This topic has been the subject of experimental studies by our team and I will present some unpublished results on this regard. In brief, we have evidence supporting a fast T cell response that damages the brain in an innate rather than antigen-specific way. Whether brain antigen-dependent responses occur after stroke has not been demonstrated so far, but we showed that brain-?derived antigens are found in lymphoid tissue of stroke patients. Overall, it is now apparent that stroke alerts the immune system and that immune responses contribute to stroke brain damage.
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