Thymic epithelial cells (TECs) play a crucial role in the immune system by selecting T cells that can protect the body while maintaining self-tolerance. This article explores how TECs amplify chromatin accessibility fluctuations, or ‘epigenetic noise’, during their maturation process. These fluctuations destabilize chromatin, leading to the ectopic expression of genes that are typically restricted to other tissues. Interestingly, this process doesn’t depend on the transcriptional activator AIRE but rather on the repression of the tumor suppressor p53. By enhancing p53 activity, TECs stabilize chromatin, limit their plasticity, and cause autoimmune reactions. The study reveals that chromatin destabilization in thymic epithelial cells is linked to elevated DNA damage and transcriptional initiation. The findings also highlight the molecular mechanisms behind thymic epithelial plasticity and their impact on immunological tolerance. These insights could be crucial for understanding autoimmune diseases and could have implications for therapeutic approaches to autoimmune disorders.
Original title: Thymic epithelial cells amplify epigenetic noise to promote immune tolerance
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