LAUSR

Aims: Fc&ggr; receptor I (Fc&ggr;RI/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 Fc&ggr;RI is positively correlated with immune inflammation. The primary aim of this study was to explore the effects of Fc&ggr;RI expression on immune‐related inflammatory response and investigate the potential mechanisms. Main methods: Fc&ggr;RI‐expressing Ba/F3 cells are the ideal models for evaluating the functions of Fc&ggr;RI. Nuclear factor kappa B (NF‐&kgr;B) and NOD‐like receptor protein 3 (NLRP3) inflammasome‐associated protein expressions and inflammatory cytokine (IL‐1&bgr; and IL‐18) release were detected in the presence or absence of NF‐&kgr;B inhibitor pyrrolidine dithiocarbamate (PDTC). Besides, the effects of Fc&ggr;RI on the activation of the NLRP3 inflammasomes were also investigated in THP‐1 macrophages deficient for Fc&ggr;RI. Key findings: Fc&ggr;RI‐expressing Ba/F3 cells appeared increased NLRP3 inflammasome formation and IL‐1&bgr; and IL‐18 release via activating NF‐&kgr;B signaling. Interestingly, this alteration could be reversed in THP‐1 macrophages after Fc&ggr;RI was silenced. Significance: These results indicated that Fc&ggr;RI functioned as a regulator for immune inflammation via acceleration of NF‐&kgr;B regulating NLRP3 inflammasome signaling.