CCL2, but not its receptor, is essential to restrict immune privileged central nervous system‐invasion of Japanese encephalitis virus via regulating accumulation of CD11b+ Ly‐6Chi monocytes
CCR2
DOI:
10.1111/imm.12626
Publication Date:
2016-06-04T15:39:23Z
AUTHORS (10)
ABSTRACT
Summary Japanese encephalitis virus ( JEV ) is a re‐emerging zoonotic flavivirus that poses an increasing threat to global health and welfare due rapid changes in climate demography. Although the CCR 2– CCL 2 axis plays important role trafficking CD 11b + Ly‐6C hi monocytes regulate immunopathological diseases, little known about their monocyte during viral caused by infection. Here, we explored of its ligand JE infection using 2‐ 2‐ablated murine models. Somewhat surprisingly, ablation resulted starkly contrasting susceptibility . induced enhanced resistance , whereas highly increased This regulation progression was coupled central nervous system CNS infiltration Ly‐6G granulocytes. There also expression CC CXC chemokines mice, which appeared induce these cell populations. However, our data revealed mice unlikely be mediated innate natural killer adaptive T‐cell responses. Furthermore, produced haematopoietic stem cell‐derived leucocytes played dominant accumulation infected bone marrow chimeric models, thereby exacerbating progression. Collectively, indicate essential conferring protection against In addition, blockage 2, but not will aid development strategies for prophylactics therapeutics
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