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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

  1. Author:
    Chen, K. Q.
    Huang, J.
    Liu, Y.
    Gong, W. H.
    Cui, Y. H.
    Wang, J. M.

  2. Author Address

    Chen, Keqiang, Huang, Jian, Liu, Ying, Wang, Ji Ming] NCI, Ctr Canc Res, Mol Immunoregulat Lab, Canc & Inflammat Program, Frederick, MD 21702 USA. [Chen, Keqiang] Shanghai Jiao Tong Univ, Sch Agr & Biol, Shanghai 200030, Peoples R China. [Huang, Jian, Cui, Youhong] Third Mil Med Univ, Chongqing, Peoples R China. [Gong, Wanghua] NCI, SAIC Frederick, Frederick, MD 21702 USA.
    1. Year: 2009
  2. Journal: Journal of Neuroimmunology
    1. 213
    2. 1-2
    3. Pages: 69-77
  4. Type of Article: Article
  1. 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 1342, 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 I kappa B-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. Published by Elsevier B.V.

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  2. DOI: 10.1016/j.jneuroim.2009.05.018
  3. PMID: 19559490

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