TY  - JOUR
A1  - Chhatbar, Chintan
A1  - Detje, Claudia N.
A1  - Grabski, Elena
A1  - Borst, Katharina
A1  - Spanier, Julia
A1  - Ghita, Luca
A1  - Elliott, David A.
A1  - Jordão, Marta Joana Costa
A1  - Mueller, Nora
A1  - Sutton, James
A1  - Prajeeth, Chittappen K.
A1  - Gudi, Viktoria
A1  - Klein, Michael A.
A1  - Prinz, Marco
A1  - Bradke, Frank
A1  - Stangel, Martin
A1  - Kalinke, Ulrich
T1  - Type I Interferon Receptor Signaling of Neurons and Astrocytes Regulates Microglia Activation during Viral Encephalitis
T2  - Cell Reports
N2  - In sterile neuroinflammation, a pathological role is proposed for microglia, whereas in viral encephalitis, their function is not entirely clear. Many viruses exploit the odorant system and enter the CNS via the olfactory bulb (OB). Upon intranasal vesicular stomatitis virus instillation, we show an accumulation of activated microglia and monocytes in the OB. Depletion of microglia during encephalitis results in enhanced virus spread and increased lethality. Activation, proliferation, and accumulation of microglia are regulated by type I IFN receptor signaling of neurons and astrocytes, but not of microglia. Morphological analysis of myeloid cells shows that type I IFN receptor signaling of neurons has a stronger impact on the activation of myeloid cells than of astrocytes. Thus, in the infected CNS, the cross talk among neurons, astrocytes, and microglia is critical for full microglia activation and protection from lethal encephalitis.
KW  - encephalitis
KW  - regulation of microglia activation
KW  - neurons
KW  - astrocytes
KW  - type I IFN receptor signaling
Y1  - 2018
UR  - https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/22245
UR  - https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-222456
VL  - 25
ER  -