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Specific DNA sequence features encode the persistence of epigenetic memory of inflammation Guillaume Blot1 and Przemyslaw Sapieha1,2 Inflammation is transient, but its consequences can be lifelong. Even brief episodes of inflammation can lead to long-lasting changes in chromatin that control gene expression. These changes can poise cells to respond differently to subsequent inflammation episodes. For example, an initial encounter with environmental stressors, such as bacteria, viruses, or Western diets, durably tunes innate immune responses to later (related or unrelated) challenges (1, 2). These mechanisms also exist in nonimmune cells, including the epidermal cells of human skin (3, 4). Why some inflammation-induced chromatin alterations are transient whereas others persist is unclear. On page 1347 of this issue, Cowley et al. …
摘自《科学》(Science)第391卷 第6792期 · 2026年3月26日,Guillaume Blot and Przemyslaw Sapieha。仅引用开头一小段供了解文章,版权归原刊所有,全文请阅读原刊。