ABSTRACT
Inflammatory cell recruitment to the central nervous system (CNS) is a critical step in the evolution of pathological and host-defense processes as diverse as head trauma, stroke, viral encephalitis, and multiple sclerosis (MS). The CNS constitutes a leukocyte-deficient environment with limited regenerative capacity; these attributes require efficient response to pathogens and noxious stimuli. However, the brain and spinal cord are rigidly confined within the skull and dura, rendering catastrophic inflammatory responses that generate distention. Further, the anatomic isolation imposed by the blood-brain-barrier (BBB) has made it difficult to define how inflammatory processes within the CNS are initiated. Not surprisingly, given these attributes, CNS inflammation exhibits a distinctly regional character (Fabry et al., 1994). Recently, progress has been made in addressing general mechanisms of leukocyte extravasation into lymphoid and parenchymal tissues. These insights have been applied to the problem of inflammation in the CNS, through the exploitation of varied models of inflammation and immunopathogenesis, including experimental autoimmune encephalomyelitis (EAE) (Tani and Ransohoff, 1994).
