先天免疫系统
神经炎症
趋化因子受体
细胞生物学
炎症
CXCL10型
CCL5
CX3CL1型
细胞因子
CCL7型
CXCL2型
作者
Luca Ghita,Julia Spanier,Chintan Chhatbar,Felix Mulenge,Andreas Pavlou,Pia-Katharina Larsen,Inken Waltl,Yvonne Lueder,Moritz Kohls,Klaus Jung,Sonja M. Best,Reinhold Förster,Martin Stangel,Dietmar Schreiner,Ulrich Kalinke
出处
期刊:Science immunology
[American Association for the Advancement of Science (AAAS)]
日期:2021-06-25
卷期号:6 (60)
被引量:4
标识
DOI:10.1126/sciimmunol.abc9165
摘要
Viral encephalitis initiates a series of immunological events in the brain that can lead to brain damage and death. Astrocytes express IFN-β in response to neurotropic infection, whereas activated microglia produce proinflammatory cytokines and accumulate at sites of infection. Here, we observed that neurotropic vesicular stomatitis virus (VSV) infection causes recruitment of leukocytes into the central nervous system (CNS), which requires MyD88, an adaptor of Toll-like receptor and interleukin-1 receptor signaling. Infiltrating leukocytes, and in particular CD8+ T cells, protected against lethal VSV infection of the CNS. Reconstitution of MyD88, specifically in neurons, restored chemokine production in the olfactory bulb as well as leukocyte recruitment into the infected CNS and enhanced survival. Comparative analysis of the translatome of neurons and astrocytes verified neurons as the critical source of chemokines, which regulated leukocyte infiltration of the infected brain and affected survival.
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