Reduced macrophage infiltration and demyelination in mice lacking the chemokine receptor CCR5 following infection with a neurotropic coronavirus.
Reduced macrophage infiltration and demyelination in mice lacking the chemokine receptor CCR5 following infection with a neurotropic coronavirus.
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DOI：
10.1006/viro.2001.1050
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发表时间：
2001-09-15
期刊：
影响因子：
3.7
通讯作者：
Lane TE
中科院分区：
文献类型：
--
作者：
Glass WG;Liu MT;Kuziel WA;Lane TE
研究旨在调查 CC 趋化因子受体 CCR5 在小鼠肝炎病毒 (MHV) 颅内感染后宿主防御和疾病发展中的贡献。感染 MHV 的 CCR5−/− 小鼠在感染后第 7 天 (pi) 时 T 细胞募集受损，这与大脑内滴度的增加 (P ≤ 0.03) 相关。然而，到接种后第 12 天，受感染的 CCR5−/− 和 CCR5+/+ 小鼠的 CNS 中 T 细胞浸润相似，并且两种菌株都表现出相当的病毒滴度，表明 CCR5 表达对于宿主防御并不是必需的。 MHV 感染 CCR5+/+ 小鼠后，超过 50% 的表达 CCR5 抗原的细胞被激活的巨噬细胞/小胶质细胞（通过 F4/80 抗原表达确定）。此外，受感染的CCR5−/−小鼠表现出巨噬细胞（CD45highF4/80+）浸润减少（P≤0.02），这与与CCR5+/+小鼠相比脱髓鞘严重程度显着降低（P≤0.001）相关。这些数据表明，CCR5 通过允许巨噬细胞进入 CNS 来促进 MHV 诱导的脱髓鞘。
Studies were performed to investigate the contributions of the CC chemokine receptor CCR5 in host defense and disease development following intracranial infection with mouse hepatitis virus (MHV). T cell recruitment was impaired in MHV-infected CCR5−/− mice at day 7 postinfection (pi), which correlated with increased (P ≤ 0.03) titers within the brain. However, by day 12 pi, T cell infiltration into the CNS of infected CCR5−/− and CCR5+/+ mice was similar and both strains exhibited comparable viral titers, indicating that CCR5 expression is not essential for host defense. Following MHV infection of CCR5+/+ mice, greater than 50% of cells expressing CCR5 antigen were activated macrophage/microglia (determined by F4/80 antigen expression). In addition, infected CCR5−/− mice exhibited reduced (P ≤ 0.02) macrophage (CD45highF4/80+) infiltration, which correlated with a significant reduction (P ≤ 0.001) in the severity of demyelination compared to CCR5+/+ mice. These data indicate that CCR5 contributes to MHV-induced demyelination by allowing macrophages to traffic into the CNS.
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