Skip to main content Sign In NIP banner   Recent research in
clinical and experimental stroke  indicates that inflammation is
a major contributor to injury and that immune cells (such as
neutrophils, macrophages and lymphocytes) infiltrate into the
brain and directly participate in ischemia-induced cell death.
Similarly, a role for inflammation is evident following global
cerebral ischemia, as experienced following CA/CPR, however the
brain resident microglia are implicated in this response. Our
recent data demonstrate for the first time that cardiac arrest-
induced cerebral ischemia stimulates rapid infiltration of T
lymphocytes into the brain and that inhibiting the activity of
these cells reoresents a novel approach to minimizing injury.
Most surprisingly, the majority of T cells in the brain
following CA/CPR are a unique T cell subset (CD4loCD40+ referred
to as Th40) that are known contributors to various autoimmune
conditions including type 1 diabetes and multiple sclerosis. 
This collaboration with Dr. W