کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3064980 1580460 2009 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
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
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
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
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 213, Issues 1–2, 18 August 2009, Pages 69–77
نویسندگان
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