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前沿速递 | ncs 集萃：2026-09-24 期
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BC200基因逃逸至人类痘病毒揭示其在灵长类动物中的持续转座
Escape of the BC200 gene to a human poxvirus reveals its persistent transposition in primates
Transposable elements mobilize within and occasionally between genomes, including from host to virus. We identified two insertions of the human BC200 noncoding RNA gene in the poxvirus molluscum contagiosum virus (MCV), which were likely acquired through long interspersed nuclear element 1 (LINE-1 or L1)–mediated retrotransposition during modern human history. Although BC200 was co-opted approximately 40 million years ago to regulate neuronal translation, we show that it never lost its mobilizat
转座元件可在基因组内及不同基因组间（包括从宿主到病毒）移动，研究发现人类BC200非编码RNA基因的两个插入片段存在于传染性软疣病毒中，这些片段可能是在现代人类历史时期通过长散在核元件1（LINE-1或L1）介导的逆转录转座作用获得的；尽管BC200约4000万年前被用于调节神经元翻译，但其从未丧失移动能力，反而在类人猿进化过程中作为“主”来源驱动了数百个谱系特异性L1介导的生殖细胞逆转录转座事件，并在人类群体中产生了可遗传的多态性插入（包括个体特异性的持续转座活动），最终近期逃逸至人类痘病毒中。
人类BC200非编码RNA基因兼具稳定功能与持续转座活性，不仅驱动类人猿进化中的生殖细胞逆转录转座，还在人类群体中形成多态性插入并逃逸至痘病毒。
成纤维细胞通过胰岛素样生长因子1依赖性调节先天淋巴细胞抑制肠道炎症
Fibroblasts restrain gut inflammation by IGF1-dependent regulation of innate lymphocytes
Fibroblasts exhibit phenotypic and functional heterogeneity in chronic inflammatory diseases, but how these changes impact immune outcomes remains poorly understood. We identified that a fibroblast population expressing insulin-like growth factor 1 (IGF1) was reduced in patients with inflammatory bowel disease (IBD). Using mouse models of intestinal inflammation, we found cross-talk between IGF1-expressing fibroblasts and group 3 innate lymphoid cells (ILC3s). IGF1 stimulation limited the abilit
成纤维细胞在慢性炎症性疾病中表现出表型和功能异质性，但这些变化如何影响免疫结果仍知之甚少。本研究发现，炎性肠病（IBD）患者的胰岛素样生长因子1（IGF1）表达型成纤维细胞数量减少；通过小鼠肠道炎症模型证实，IGF1表达型成纤维细胞与3型先天淋巴细胞（ILC3s）存在相互作用，IGF1刺激可抑制ILC3产生CXCL10并招募浆细胞样树突状细胞（pDC），从而减轻肠道炎症；该调控通路在人类ILC3中保守但在IBD中可能受损，表明抗炎性成纤维细胞通过调节先天淋巴细胞-pDC轴保护肠道。
IGF1表达型成纤维细胞通过抑制ILC3的CXCL10分泌和pDC招募来缓解肠道炎症，这一机制在IBD患者中受损。