SNX25 通过 NF-κB 信号调节巨噬细胞中促炎细胞因子的表达。

Department of Anatomy and Neuroscience, Nara Medical University, Kashihara, Nara, Japan.

PLoS One. 2021 Mar 1;16(3):e0247840. doi: 10.1371/journal.pone.0247840. eCollection 2021.

Innate immunity is the first line of defense against bacterial infection and is initiated by macrophages. Sorting nexin 25 (SNX25) is an SNX family member and is reported to negatively regulate TGF-β signaling by enhancing TGF receptor degradation. However, few studies have focused on the relationship between SNX25 and the immune system. We knocked down SNX25 expression in macrophages and examined inflammatory cytokine expression, a hallmark of innate immunity, after lipopolysaccharide stimulation. SNX25 knockdown increased proinflammatory cytokine expression in RAW 264.7 cells. In addition, SNX25 knockdown activated the NF-κB signal by promoting ubiquitination of IκBα. These results suggest that SNX25 inhibits the NF-κB signal and thereby regulates proinflammatory cytokine expression in macrophages.

先天免疫是抵御细菌感染的第一道防线，由巨噬细胞启动。分选连接蛋白 25（SNX25）是 SNX 家族的一员，据报道通过增强 TGF 受体降解来负调控 TGF-β信号。然而，很少有研究关注 SNX25 与免疫系统之间的关系。我们敲低了巨噬细胞中的 SNX25 表达，并在脂多糖刺激后检测了先天免疫的标志之一炎症细胞因子的表达。SNX25 敲低增加了 RAW 264.7 细胞中促炎细胞因子的表达。此外，SNX25 敲低通过促进 IκBα的泛素化激活了 NF-κB 信号。这些结果表明，SNX25 抑制 NF-κB 信号，从而调节巨噬细胞中促炎细胞因子的表达。