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 Neuroimmunoljournal_title
Journal of neuroimmunologyauthors
Zhou S,Halle A,Kurt-Jones EA,Cerny AM,Porpiglia E,Rogers M,Golenbock DT,Finberg RWdoi
10.1016/j.jneuroim.2007.11.018subject
Has Abstractpub_date
2008-02-01 00:00:00pages
70-82issue
1-2eissn
0165-5728issn
1872-8421pii
S0165-5728(07)00430-4journal_volume
194pub_type
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