microglial precursors recruited in a pathogenic manner in West Nile virus encephalitis

The Rockefeller University Press $30.00 J. Exp. Med. www.jem.org/cgi/doi/10.1084/jem.20080421 Cite by DOI: 10.1084/jem.20080421 1 of 19 The mechanism resulting in increased numbers of microglia in the central nervous system (CNS) during infl ammation has long been debated. Microglia have been shown to proliferate in situ in several synthetic infl ammatory models ( 1 – 4 ). In contrast, it is suggested that microglia can diff erentiate from blood-derived precursors that migrate into the CNS; however, recent reports suggest that this can only occur after radiation-induced “ preconditioning ” of the brain ( 5 – 10 ). Whether viral infection initiates events resulting in microglial recruitment from the periphery is unknown. During embryonic development, microglia populate the CNS from myeloid lineage precursors in the BM ( 11 ). Much is known about early monocyte lineage precursors, but the diff erentiation to downstream eff ector populations in the adult remain poorly defi ned. Geissman et al. ( 13 ) have described two major subsets in the peripheral blood, the “ infl ammatory ” and “ circulating ” monocyte ( 12, 14 ). Infl ammatory monocytes express Ly6C hi (Gr1) and the chemokine receptor CORRESPONDENCE Nicholas J.C. King: [email protected]