A20 is a potent anti-inflammatory protein, acting by inhibiting nuclear factor κB (NF-κB) signaling and inflammatory gene expression and/or by preventing cell death. Mutations in the A20/TNFAIP3 gene have been associated with a plethora of inflammatory and autoimmune pathologies in humans and in mice. Although the anti-inflammatory role of A20 is well accepted, fundamental mechanistic questions regarding its mode of action remain unclear. Here, we review new findings that further clarify the molecular and cellular mechanisms by which A20 controls inflammatory signaling and cell death, and discuss new evidence for its involvement in inflammatory and autoimmune disease development.

中文翻译：

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A20 处于细胞死亡、炎症和自身免疫的十字路口。

A20 是一种有效的抗炎蛋白，通过抑制核因子 κB (NF-κB) 信号传导和炎症基因表达和/或通过防止细胞死亡来发挥作用。A20/TNFAIP3 基因的突变与人类和小鼠的大量炎症和自身免疫病理有关。尽管 A20 的抗炎作用已被广泛接受，但关于其作用方式的基本机制问题仍不清楚。在这里，我们回顾了进一步阐明 A20 控制炎症信号传导和细胞死亡的分子和细胞机制的新发现，并讨论了其参与炎症和自身免疫性疾病发展的新证据。