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Differences in TLR7/8 activation between monocytes and macrophages

Journal Article · · Biochemical and Biophysical Research Communications
;  [1];  [2]
  1. Department of Pathology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, 833 (China)
  2. Department of Medical Research, E-DA Hospital/I-Shou University, Kaohsiung, 824 (China)
Highlights: • Only TLR8 agonists induced NF-κB and ISG activation in monocytes. • TLR8 could inhibit TLR7-induced NF-κB activation in monocytes. • Both TLR7 and TLR8 agonists only induced NF-κB but not ISG activation in macrophages. • Differences in expression levels of molecules involved in TLR signaling between monocytes and macrophages. • Comparison between monocytes and macrophages in expression levels of molecules after TLR7/8 activation. The recognition of single-stranded RNA by TLR7/8 leads to the production of NF-κB-mediated cytokines and type I IFNs. However, the role of TLR7/8 activation in monocytes and macrophages is still unclear. The aim of this study was to investigate the differences in the activation of TLR7/8 between these two cell types. Microarray analysis, qRT-PCR and flow cytometry were used to analyse TLR7/8 signalling pathways in monocytes and macrophages after stimulation with agonists. Our data indicated that TLR8 agonists activated the NF-κB- and IRF-mediated pathways in THP-1 cells, whereas TLR7 agonists did not. However, silent TLR8 and enhanced TLR7 expression could increase TLR7-induced NF-κB activation in monocytes. TLR7 and TLR8 agonists induced NF-κB activation but no ISG response in PMA-differentiated THP-1 cells. The mRNA levels of pro-inflammatory cytokine were elevated upon CL075 stimulation in macrophages compared to monocytes. Thus, TLR7 and TLR8 might modulate different immune responses in monocytes and macrophages.
OSTI ID:
23137330
Journal Information:
Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 497; ISSN 0006-291X; ISSN BBRCA9
Country of Publication:
United States
Language:
English

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