Article ID Journal Published Year Pages File Type
3064980 Journal of Neuroimmunology 2009 9 Pages PDF
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 β42, 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 IκB-α 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.

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