Hongfeng Zhang1, Ling Li2, Lei Liu2. 1. Department of Rheumatology and Immunology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116001, People's Republic of China. Electronic address: zhf20160727@163.com. 2. Department of Rheumatology and Immunology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116001, People's Republic of China.
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.
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.
Authors: Katarína Matiašková; Lenka Kavanová; Pavel Kulich; Jan Gebauer; Kateřina Nedbalcová; Hana Kudláčková; Radek Tesařík; Martin Faldyna Journal: Front Immunol Date: 2021-04-22 Impact factor: 7.561