A20 is a potent anti-inflammatory molecule, and mutations in TNFAIP3, the gene encoding A20, are associated with a wide panel of inflammatory pathologies, both in human and mouse. The anti-inflammatory properties of A20 are commonly attributed to its ability to suppress inflammatory NF-κB signaling by functioning as a ubiquitin-editing enzyme. However, A20 also protects cells from death, independently of NF-κB regulation, and recent work has demonstrated that cell death may drive some of the inflammatory conditions caused by A20 deficiency. Adding to the fact that the protective role of A20 does not primarily rely on its catalytic activities, these findings shed new light on A20 biology.

中文翻译：

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A20 和细胞死亡驱动的炎症。

A20 是一种有效的抗炎分子，编码 A20 的基因 TNFAIP3 的突变与人类和小鼠的多种炎症病理相关。A20 的抗炎特性通常归因于其作为泛素编辑酶抑制炎症 NF-κB 信号传导的能力。然而，A20 还可以独立于 NF-κB 调节而保护细胞免于死亡，最近的研究表明，细胞死亡可能会导致一些由 A20 缺乏引起的炎症。A20 的保护作用并不主要依赖于其催化活性，这些发现为 A20 生物学提供了新的线索。