Ly6c+ inflammatory monocytes

Ly6c+ inflammatory monocytes - Published September 8, 2008...

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The Journal of Experimental Medicine ARTICLE The Rockefeller University Press $30.00 J. Exp. Med. Vol. 205 No. 10 2319-2337 2319 The mechanism resulting in increased numbers of microglia in the central nervous system (CNS) during inF ammation has long been de- bated. Microglia have been shown to prolifer- ate in situ in several synthetic inF ammatory models ( 1 – 4 ). In contrast, it is suggested that microglia can di± erentiate from blood-derived precursors that migrate into the CNS; how- ever, 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 precur- sors in the BM ( 11 ). Much is known about early monocyte lineage precursors, but the di± erentia- tion to downstream e± ector populations in the adult remain poorly de² ned. Geissman et al. ( 13 ) have described two major subsets in the periph- eral blood, the “ inF ammatory ” and “ circulating ” monocyte ( 12, 14 ). InF ammatory monocytes ex- press Ly6C hi (Gr1) and the chemokine receptor CORRESPONDENCE Nicholas J.C. King: ± Abbreviations used: ANOVA, analysis of variance; BBB, blood-brain barrier; C-L, clo- dronate-loaded; CNS, central nervous system; D-L, Dil-la- beled; H & E, hematoxylin and eosin; IHC, immunohistochem- istry; p.i., postinfection; WNV, West Nile virus. D.R. Getts ’ present address is Department of Microbiology and Immunology, Northwestern University, Chicago, IL. B. Shrestha ’ s present address is Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110. M. M ü ller ’ s present address is Department of Neurology, University of Bonn, 53105 Bonn, Germany. The online version of this article contains supplemental material. Ly6c + inf ammatory monocytes ” are microglial precursors recruited in a pathogenic manner in West Nile virus encephalitis Daniel R. Getts , 1,2 Rachael L. Terry , 1,2 Meghann Teague Getts , 1,2 Marcus M ü ller , 3 Sabita Rana , 1,2 Bimmi Shrestha , 1 Jane RadFord , 1,2 Nico Van Rooijen , 3,4 Iain L. Campbell , 2,3 and Nicholas J.C. King 1,2 1 The Discipline of Pathology, School of Medical Sciences, 2 Bosch Institute, Faculty of Medicine, and 3 School of Molecular and Microbial Biosciences, Faculty of Science, The University of Sydney, Sydney NSW 2006, Australia 4 Department of Molecular Cell Biology, Faculty of Medicine, Vrije Universiteit Medical Center, Vrije Universiteit, 1007 MB Amsterdam, Netherlands In a lethal West Nile virus (WNV) model, central nervous system infection triggered a threefold increase in CD45 int /CD11b + /CD11c ± microglia at days 6 – 7 postinfection (p.i.). Few microglia were proliferating, suggesting that the increased numbers were derived from a migratory precursor cell. Depletion of “ circulating ” (Gr1 ± (Ly6C lo )CX3CR1 + ) and in± amma- tory ” (Gr1 hi /Ly6C hi /CCR2 + ) classical monocytes during infection abrogated the increase in microglia. C57BL/6 chimeras reconstituted with cFMS – enhanced green ±
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Ly6c+ inflammatory monocytes - Published September 8, 2008...

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