The pathology of a stroke is deceptively complicated. In the simplest sense, strokes occur when the blood supply to a particular region of the brain is interrupted, cutting off the area to oxygen and nutrients. This deprivation results in injury and death to the local brain cells.
But for days after the breach in blood flow, the immune system also does its own fair share of damage to the already injured brain through an inflammatory response. New research by a group at Stanford University has identified a subset of immune cells that drive brain injury following a stroke, raising the possibility that immune-system inhibition might be a promising treatment for a blood-deprived brain.
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Myeloid cell surfaces bear a molecule called TREM1, or triggering receptor expressed on myeloid cells 1, that amplifies immune responses. Normally TREM1 drives the immune system to fight infections, but when it is too aggressive, it can contribute not just to stroke but to other serious conditions, such as heart disease and cancer.
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When mice in which the TREM1 gene had been deleted were subjected to a stroke, they had significantly less damage to their brains and exhibited higher survival rates.
Read full, original post: New Method for Tackling Stroke Restrains an Overactive Immune System
