交叉展示
生物
细胞生物学
转录因子
细胞毒性T细胞
抗原呈递
CD8型
平衡
小RNA
T细胞
抗原
免疫学
免疫系统
基因
生物化学
体外
作者
Yan Wang,Quan Zhang,Tingting He,Yechen Wang,Tianqi Lu,Zengge Wang,Yiyi Wang,Lin Shen,Kang Yang,Xinming Wang,Jun Xie,Ying Zhou,Yazhen Hong,Wen‐Hsien Liu,Kairui Mao,Shih‐Chin Cheng,Xin Chen,Qiyuan Li,Nengming Xiao
标识
DOI:10.1038/s41467-023-42428-7
摘要
Type 1 conventional dendritic cells (cDC1) are the most efficient cross-presenting cells that induce protective cytotoxic T cell response. However, the regulation of their homeostasis and function is incompletely understood. Here we observe a selective reduction of splenic cDC1 accompanied by excessive cell death in mice with Zeb1 deficiency in dendritic cells, rendering the mice more resistant to Listeria infection. Additionally, cDC1 from other sources of Zeb1-deficient mice display impaired cross-presentation of exogenous antigens, compromising antitumor CD8+ T cell responses. Mechanistically, Zeb1 represses the expression of microRNA-96/182 that target Cybb mRNA of NADPH oxidase Nox2, and consequently facilitates reactive-oxygen-species-dependent rupture of phagosomal membrane to allow antigen export to the cytosol. Cybb re-expression in Zeb1-deficient cDC1 fully restores the defective cross-presentation while microRNA-96/182 overexpression in Zeb1-sufficient cDC1 inhibits cross-presentation. Therefore, our results identify a Zeb1-microRNA-96/182-Cybb pathway that controls cross-presentation in cDC1 and uncover an essential role of Zeb1 in cDC1 homeostasis.
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