The ubiquitin-binding endoribonuclease N4BP1 is a critical immunosuppressor, but the mechanism by which it acts to constrain TLR-induced inflammatory cytokine production has remained unclear. In this issue of Immunity, Gitlin et al. find that N4BP1 works in concert with the non-canonical IκB kinase (IKK) to limit activity of the IKK complex.

中文翻译：

---

非规范 IKK 站在 N4BP1 一边反对家族

泛素结合核糖核酸内切酶 N4BP1 是一种重要的免疫抑制剂，但其抑制 TLR 诱导的炎症细胞因子产生的机制仍不清楚。在本期《 Immunity 》中，Gitlin 等人。发现 N4BP1 与非经典 IκB 激酶 (IKK) 协同作用，限制 IKK 复合物的活性。