CpG-containing oligodeoxynucleotide promotes microglial cell uptake of amyloid β 1-42 peptide by up-regulating the expression of the G-protein- coupled receptor mFPR2 Pablo Iribarren * , Keqiang Chen * , Jinyue Hu * , Wanghua Gong † , Edward H. Cho ‡ , Stephen Lockett ‡ , Badarch Uranchimeg § and Ji Ming Wang * * Laboratory of Molecular Immunoregulation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, Maryland, USA; † Basic Research Program, ‡ Image Analysis Laboratory, and § Developmental Therapeutics Program, Tumor Hypoxia Laboratory, SAIC-Frederick, Frederick, Maryland, USA 1 Correspondence: Laboratory of Molecular Immunoregulation, Center for Cancer Research, National Cancer Institute at Frederick, Bldg. 560, Room 31-40, Frederick, MD 21702-1201, USA. E-mail: wangji@mail.ncifcrf.gov <h3>SPECIFIC AIMS</h3> Inflammation contributes to the pathogenic process of Alzheimer’s disease (AD). We previously discovered that a human G-protein-coupled formyl peptide receptor-like 1 (FPRL1) and its mouse homologue mFPR2 mediate the chemotaxis and activation of mononuclear phagocytes in response to a variety of peptide agonists, including amyloid β 1-42 (Aβ 42 ), which is neurotoxic and a key mediator of inflammatory responses in AD. Since mFPR2 is up-regulated in mouse microglia by lipopolysaccharide (LPS), a Toll-like receptor 4 ligand, the aim of
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