Background and Purpose—Cerebral ischemia is associated with inflammation involving accumulation of polymorphonuclearneutrophils. T cells have been suggested to contribute to the secondary progression of ischemic braininjury. Dendritic cells (DC) are potent regulators of immunity by activating and tolerizing T cells. DC have previouslybeen detected in rat meninges and choroid plexus. Hypothesizing that DC are involved in inflammation associated withcerebral ischemia, we investigated DC in the brain of Sprague-Dawley rats after permanent middle cerebral arteryocclusion (pMCAO) versus sham operation.Methods-All experimental rats (n 24) had the right MCA permanently occluded by inserting a nylon monofilamentthrough the right external carotid artery. Immunohistochemistry was used to detect DC (OX62), microglia/macrophages (OX42) that developed into DC, and activated DC expressing major histocompatibility complex class II (OX6) in the brain hemispheres at 1 hour to 6 days after pMCAO or sham operation.Results—Levels of DC were elevated at 1 hour in the ischemic versus sham hemispheres (P 0.001) and ischemic versusnonischemic hemispheres (P 0.001). Activated DC expressing major histocompatibility complex class II(OX62 OX6 ) were still elevated at 6 days after pMCAO in the ischemic versus nonischemic hemispheres (P 0.01).The area of brain lesion correlated with numbers of OX62 DC per 100-mm2 brain tissue section (r 0.79; P 0.0001). Conclusions-Increased levels of DC inthe brain after pMCAO and correlation between DC numbers and brain lesion areaindicate a role for DC in cerebral ischemia. This observation could constitute a basis for further studies on the role ofDC in inflammation related to cerebral ischemia.