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. Wagner, who is a leader in the Th40 T cell field is aimed at assessing the role of these new effector cells, and other infiltrating immune cells, in ischemic neuronal injury.