Lymphocytic choriomeningitis virus (LCMV) infection of CNS glial cells results in TLR2-MyD88/Mal-dependent inflammatory responses.

Abstract:

:In response to invading pathogens, Toll-like receptors (TLR) play a critical role in the initiation of the innate immune response, which can be either beneficial or detrimental to the host. In the present study, we demonstrated that central nervous system (CNS) glial cells are activated by Lymphocytic Choriomeningitis Virus (LCMV) in a TLR2-MyD88/Mal-dependent manner. Specifically, in response to LCMV, both astrocytes and microglial cells isolated from wild-type (WT) mice produced chemokines, such as MCP-1, RANTES and TNF-alpha. Similar responses occurred in TLR3 KO and TLR4 KO glial cells. In striking contrast, both astrocytes and microglial cells isolated from mice deficient in TLR2, MyD88, and Mal did not produce any of these chemokines. In addition, LCMV infection of glial cells induced up-regulation of TLR2, MHC class-I and II, CD40, CD86 in a MyD88-dependent manner. These results define a functional role for TLR signaling in viral infection-induced activation of CNS glial cells as well as for the immunopathology in the CNS.

journal_name

J Neuroimmunol

authors

Zhou S,Halle A,Kurt-Jones EA,Cerny AM,Porpiglia E,Rogers M,Golenbock DT,Finberg RW

doi

10.1016/j.jneuroim.2007.11.018

subject

Has Abstract

pub_date

2008-02-01 00:00:00

pages

70-82

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(07)00430-4

journal_volume

194

pub_type

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