{"title":"弱增强子允许 Irf8 自动激活，以控制 cDC1 和 cDC2 的血统定向","authors":"","doi":"10.1038/s41590-024-01977-9","DOIUrl":null,"url":null,"abstract":"The Irf8 +32-kb enhancer controls transcriptional autoactivation to generate ‘IRF8 on’ and ‘IRF8 off’ states that define type 1 conventional dendritic cell (cDC1) and cDC2 lineages, respectively. Weak affinity of this enhancer for BATF3–JUNB–IRF8 complexes allows specified cDC2 progenitors to successfully turn off Irf8 transcription. If this enhancer is made stronger, cDC2 commitment and cDC1–cDC2 lineage segregation are compromised.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":27.7000,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Weak enhancer allows autoactivation of Irf8 to control cDC1 versus cDC2 lineage commitment\",\"authors\":\"\",\"doi\":\"10.1038/s41590-024-01977-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The Irf8 +32-kb enhancer controls transcriptional autoactivation to generate ‘IRF8 on’ and ‘IRF8 off’ states that define type 1 conventional dendritic cell (cDC1) and cDC2 lineages, respectively. Weak affinity of this enhancer for BATF3–JUNB–IRF8 complexes allows specified cDC2 progenitors to successfully turn off Irf8 transcription. If this enhancer is made stronger, cDC2 commitment and cDC1–cDC2 lineage segregation are compromised.\",\"PeriodicalId\":19032,\"journal\":{\"name\":\"Nature Immunology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":27.7000,\"publicationDate\":\"2024-10-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Immunology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41590-024-01977-9\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41590-024-01977-9","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
Weak enhancer allows autoactivation of Irf8 to control cDC1 versus cDC2 lineage commitment
The Irf8 +32-kb enhancer controls transcriptional autoactivation to generate ‘IRF8 on’ and ‘IRF8 off’ states that define type 1 conventional dendritic cell (cDC1) and cDC2 lineages, respectively. Weak affinity of this enhancer for BATF3–JUNB–IRF8 complexes allows specified cDC2 progenitors to successfully turn off Irf8 transcription. If this enhancer is made stronger, cDC2 commitment and cDC1–cDC2 lineage segregation are compromised.
期刊介绍：
Nature Immunology is a monthly journal that publishes the highest quality research in all areas of immunology. The editorial decisions are made by a team of full-time professional editors. The journal prioritizes work that provides translational and/or fundamental insight into the workings of the immune system. It covers a wide range of topics including innate immunity and inflammation, development, immune receptors, signaling and apoptosis, antigen presentation, gene regulation and recombination, cellular and systemic immunity, vaccines, immune tolerance, autoimmunity, tumor immunology, and microbial immunopathology. In addition to publishing significant original research, Nature Immunology also includes comments, News and Views, research highlights, matters arising from readers, and reviews of the literature. The journal serves as a major conduit of top-quality information for the immunology community.
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
