Abstract

The normal central nervous system (CNS) has long been believed to be an immunologically privileged site, because it is isolated from the systemic circulation, and is able to exclude components of the immune system by the blood—brain barrier (BBB) (1). The CNS constitutes a leukocyte-deficient environment with limited regenerative capacity (2). Although recent evidence suggests that the CNS is continuously patrolled by a small number of T-lymphocytes, and that certain cells of macrophage lineage (perivascular cells) are slowly replaced by hematogenous cells (3), this notion is principally true, and other immune cells, such as polymorphonuclear leukocytes (PMNLs) and monocytes, migrate only in response to tissue damage in the CNS. The infiltration of these immune cells into the CNS is a critical step in the evolution of pathological and host defense processes of various neurological diseases, such as cerebral ischemia, hemorrhage, trauma, bacterial or viral infection, and multiple sclerosis (4). In these pathological settings, the infiltration of hematogenous cells is added to the local inflammatory response composed of activation of resident microglia and astrocytes.

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