Mechanism of hyperinflammation in chronic granulomatous disease: mouse iPS cells expressing human gp91phox

我们研究了慢性肉芽肿病患者过度炎症的潜在机制。我们的数据表明，NADPH氧化酶产生的活性氧通过NLRP3炎性体和NF_κB信号通路抑制脂多糖诱导的炎症细胞因子的产生，而单核细胞在免疫应答中起核心作用。虽然需要进一步的工作来阐明CGD患者过度炎症的机制，但这一数据表明，NADPH氧化酶产生的活性氧的减少会导致炎症细胞因子的产生失调。

We investigated an underlying mechanisms of excessive inflammation in patients with chronic granulomatous disease. Our data suggested that reactive oxygen species generated by NADPH oxidase suppressed the lipopolysaccharide-induced inflammatory cytokine production through NLRP3 inflammasome and NF_κB signaling pathway in monocytes that play a central role of immune response. Although further works are required to clarify the mechanisms of excessive inflammation in CGD patients, this data indicates that reduction of reactive oxygen species generated by NADPH oxidase would induce dysregulated production of inflammatory cytokines.