Synergy of TRIF-dependent TLR3 and MyD88-dependent TLR7 in up-regulating expression of mouse FPR2, a promiscuous G-protein-coupled receptor, in microglial cells.

Abstract:

:Human G-protein-coupled formyl peptide receptor-like 1 and its mouse homologue formyl peptide receptor 2 mediate the chemotactic activity of a variety of pathogen and host-derived peptides, including amyloid beta(42), a key causative factor in Alzheimer's disease (AD).Here, we found that polyinosine-polycytidylic acid (Poly(I:C)), which is a specific TLR3 ligand, and Imiquimod (R837), which is a specific TLR7 ligand, when used alone, each increased MAPK-dependent functional mFPR2 expression in microglial cells, and the combination of Poly(I:C) and R837 exhibited additive effect by enhancing the level of IkappaB-alpha phosphorylation. Our results indicated that RNA virus infection may actively participate in the pathogenic processes of brain inflammation and neurodegenerative diseases by TLR3- and TLR7-mediated TRIF-dependent and MyD88-dependent signaling pathways.

journal_name

J Neuroimmunol

authors

Chen K,Huang J,Liu Y,Gong W,Cui Y,Wang JM

doi

10.1016/j.jneuroim.2009.05.018

subject

Has Abstract

pub_date

2009-08-18 00:00:00

pages

69-77

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(09)00213-6

journal_volume

213

pub_type

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