表观遗传学
生物
转录组
微生物群
免疫系统
免疫学
DNA甲基化
细胞生物学
主要组织相容性复合体
MHC I级
增强子
遗传学
转录因子
免疫
微阵列
肠道菌群
重编程
基因表达调控
肠-脑轴
表观遗传学
记忆B细胞
粘膜免疫学
泛素连接酶
基因表达
转录调控
细胞分化
基因表达谱
神经发生的表观遗传调控
微阵列分析技术
先天免疫系统
作者
Liu Yang,Robert C. Peery,Shirui Zhou,Xiaomin Chen,Leah M. Farmer,Fabiola Gutierrez,Stephanie Fowler,Lanjing Zhang,Julia M. Salamat,Karen Riggins,Jiejun Shi,Lanlan Shen
标识
DOI:10.1038/s41564-026-02295-6
摘要
During weaning, the transition to solid food diversifies the gut microbiome, triggering a programmed immune response critical for long-lasting mucosal immunity. Previous work showed that the gut microbiome mediates epigenetic development in intestinal stem cells (ISCs) during suckling, but what happens during weaning is unclear. Here, genome-wide profiling revealed that weaning-driven microbiome changes shape the DNA methylome and transcriptome of murine ISCs in an IFNγ-dependent manner. Specifically, we observe demethylation of enhancer elements essential for MHC class II genes, which results in a transcriptional memory that persists through differentiation into adulthood. IFNγ blockade, or low-dose penicillin to target Gram-positive bacteria, in early life impaired microbiome-mediated epigenetic control and mucosal immunity, and exacerbated colitis. Murine organoids primed with IFNγ showed rapid, amplified transcriptional responses upon secondary stimulations. These findings reveal that early-life events alter the gut microbiome and these changes reprogramme ISC epigenetic memory to shape mucosal immunity.
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