弱增强子允许 Irf8 自动激活，以控制 cDC1 和 cDC2 的血统定向

IF 27.7 1区医学 Q1 IMMUNOLOGY

Nature Immunology Pub Date : 2024-10-15 DOI:10.1038/s41590-024-01977-9

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引用次数: 0

摘要

Irf8 +32-kb增强子控制转录自激活，产生 "IRF8开启 "和 "IRF8关闭 "状态，分别定义了1型常规树突状细胞（cDC1）和cDC2系。这种增强子对 BATF3-JUNB-IRF8 复合物的亲和力较弱，因此特定的 cDC2 祖细胞能成功关闭 Irf8 转录。如果该增强子变得更强，cDC2 的承诺和 cDC1-cDC2 系的分离就会受到影响。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Weak enhancer allows autoactivation of Irf8 to control cDC1 versus cDC2 lineage commitment

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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.

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来源期刊

Nature Immunology 医学-免疫学

CiteScore

40.00

自引率

2.30%

发文量

248

审稿时长

4-8 weeks

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.