Ly6c+ "inflammatory monocytes" are microglial precursors recruited in a pathogenic manner in West Nile virus encephalitis.
Ly6c+ "inflammatory monocytes" are microglial precursors recruited in a pathogenic manner in West Nile virus encephalitis.
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LY6C+“炎症单核细胞”是在西尼罗河病毒脑炎中以致病方式募集的小胶质前体。
DOI：
10.1084/jem.20080421
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发表时间：
2008-09-29
期刊：
影响因子：
--
通讯作者：
King NJ
中科院分区：
文献类型：
--
作者：
Getts DR;Terry RL;Getts MT;Müller M;Rana S;Shrestha B;Radford J;Van Rooijen N;Campbell IL;King NJ
在致命的西尼罗河病毒（WNV）模型中，中枢神经系统感染在感染后6-7天（p.i.）触发了CD 45 int/CD 11b +/CD 11 c −小胶质细胞的三倍增加。很少有小胶质细胞增殖，这表明增加的数量来自迁移前体细胞。在感染过程中，“循环”（Gr 1 −（Ly 6Clo）CX 3CR 1+）和“炎性”（Gr 1hi/Ly 6Chi/CCR 2+）经典单核细胞的消耗消除了小胶质细胞的增加。用cFMS增强的绿色荧光蛋白（EGFP）重建的C57 BL/6嵌合体骨髓（BM）在感染后第7天显示出大量表达GR 1+（Ly 6 C+）的外周来源的（GFP+）小胶质细胞，表明炎性单核细胞是小胶质细胞前体。这通过过继转移标记的BM（Ly 6Chi/CD 115+）或循环炎性单核细胞来证实，所述循环炎性单核细胞运输到WNV感染的脑并表达小胶质细胞表型。CCL 2是一种在WNV感染期间高度表达的趋化因子，并且在炎性单核细胞运输中很重要。CCL 2的中和作用不仅减少了WNV感染期间脑中GFP+小胶质细胞的数量，而且延长了受感染动物的寿命。因此，CCL 2依赖性炎性单核细胞迁移对于WNV感染期间小胶质细胞的增加至关重要，并且在WNV脑炎期间也可能发挥致病作用。
In a lethal West Nile virus (WNV) model, central nervous system infection triggered a threefold increase in CD45int/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−(Ly6Clo)CX3CR1+) and “inflammatory” (Gr1hi/Ly6Chi/CCR2+) classical monocytes during infection abrogated the increase in microglia. C57BL/6 chimeras reconstituted with cFMS–enhanced green fluorescent protein (EGFP) bone marrow (BM) showed large numbers of peripherally derived (GFP+) microglia expressing GR1+(Ly6C+) at day 7 p.i., suggesting that the inflammatory monocyte is a microglial precursor. This was confirmed by adoptive transfer of labeled BM (Ly6Chi/CD115+) or circulating inflammatory monocytes that trafficked to the WNV-infected brain and expressed a microglial phenotype. CCL2 is a chemokine that is highly expressed during WNV infection and important in inflammatory monocyte trafficking. Neutralization of CCL2 not only reduced the number of GFP+ microglia in the brain during WNV infection but prolonged the life of infected animals. Therefore, CCL2-dependent inflammatory monocyte migration is critical for increases in microglia during WNV infection and may also play a pathogenic role during WNV encephalitis.
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