FcγRI (CD64) contributes to the severity of immune inflammation through regulating NF-κB/NLRP3 inflammasome pathway

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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.

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