Abstract：
AIMS:Fcγ receptor I (FcγRI/CD64) that is restrictedly expressed on monocytes and macrophages, acts as the single high-affinity receptor of immunoglobulin G (IgG) in human. The expression of FcγRI is positively correlated with immune inflammation. The primary aim of this study was to explore the effects of FcγRI expression on immune-related inflammatory response and investigate the potential mechanisms. MAIN METHODS:FcγRI-expressing Ba/F3 cells are the ideal models for evaluating the functions of FcγRI. Nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasome-associated protein expressions and inflammatory cytokine (IL-1β and IL-18) release were detected in the presence or absence of NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC). Besides, the effects of FcγRI on the activation of the NLRP3 inflammasomes were also investigated in THP-1 macrophages deficient for FcγRI. KEY FINDINGS:FcγRI-expressing Ba/F3 cells appeared increased NLRP3 inflammasome formation and IL-1β and IL-18 release via activating NF-κB signaling. Interestingly, this alteration could be reversed in THP-1 macrophages after FcγRI was silenced. SIGNIFICANCE:These results indicated that FcγRI functioned as a regulator for immune inflammation via acceleration of NF-κB regulating NLRP3 inflammasome signaling.
journal_name
Life Scijournal_title
Life sciencesauthors
Zhang H,Li L,Liu Ldoi
10.1016/j.lfs.2018.06.015subject
Has Abstractpub_date
2018-08-15 00:00:00pages
296-303eissn
0024-3205issn
1879-0631pii
S0024-3205(18)30356-4journal_volume
207pub_type
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