这篇文章探讨了胸腺上皮细胞（mTECs）中的细胞可塑性机制，这种可塑性对免疫耐受的建立至关重要。研究人员发现，背景染色质可及性波动的放大（称为“表观遗传噪音”）促使mTECs异位表达通常限于其他组织的基因。这种噪音与肿瘤抑制因子p53的抑制相关，而增强p53活性则能稳定染色质，限制细胞可塑性，但同时也导致了多器官自身免疫。此外，染色质可及性噪音被发现与富含AT的基因组序列以及DNA损伤和转录起始的增加有关，突显了p53间接调控染色质稳定性以维持免疫功能的作用，并在肺腺癌（LUAD）模型中进一步证明了p53对染色质噪音和表型可塑性的抑制作用。References: Gamble N, Caldwell J A, McKeever J, et al. Thymic epithelial cells amplify epigenetic noise to promote immune tolerance[J]. Nature, 2025: 1-10.
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