PDF(Pubmed)
Abstract：
Inflammatory monocytes (iMO) are recruited from the bone marrow to the brain during viral encephalitis. C-C motif chemokine receptor (CCR) 2 deficiency substantially reduces iMO recruitment for most, but not all encephalitic viruses. Here we show CCR7 acts synergistically with CCR2 to control this process. Following Herpes simplex virus type-1 (HSV-1), or La Crosse virus (LACV) infection, we find iMO proportions are reduced by approximately half in either Ccr2 or Ccr7 knockout mice compared to control mice. However, Ccr2/Ccr7 double knockouts eliminate iMO recruitment following infection with either virus, indicating these receptors together control iMO recruitment. We also find that LACV induces a more robust iMO recruitment than HSV-1. However, unlike iMOs in HSV-1 infection, LACV-recruited iMOs do not influence neurological disease development. LACV-induced iMOs have higher expression of proinflammatory and proapoptotic but reduced mitotic, phagocytic and phagolysosomal transcripts compared to HSV-1-induced iMOs. Thus, virus-specific activation of iMOs affects their recruitment, activation, and function.
摘要：
在病毒性脑炎期间,炎性单核细胞(iMO)从骨髓募集至脑。C-C基序趋化因子受体（CCR）2缺乏大大减少了大多数人的iMO募集，但不是所有的脑炎病毒.这里我们显示CCR7与CCR2协同作用以控制该过程。继单纯疱疹病毒1型（HSV-1）之后，或LaCrosse病毒（LACV）感染，我们发现与对照小鼠相比,Ccr2或Ccr7基因敲除小鼠的iMO比例降低了大约一半.然而,Ccr2/Ccr7双敲除消除感染两种病毒后的iMO募集，表明这些受体共同控制iMO募集。我们还发现LACV比HSV-1诱导更强大的iMO募集。然而,与HSV-1感染中的iMO不同，LACV招募的iMO不会影响神经系统疾病的发展。LACV诱导的iMO有较高的促炎和促凋亡表达，但有丝分裂减少，与HSV-1诱导的iMO相比，吞噬和吞噬溶酶体转录本。因此，iMO的病毒特异性激活会影响他们的招募，激活,和功能。
