Department of Oncology, Amgen Inc., South San Francisco, CA.
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.
J Immunol. 2021 Jul 1;207(1):125-132. doi: 10.4049/jimmunol.1901010. Epub 2021 Jun 16.
The transcriptional repressor has been reported as required for development of a subset of classical dendritic cell (cDCs) called cDC1, which is responsible for cross-presentation. However, mechanisms and in vivo functional analysis have been lacking. We generated a system for conditional deletion of in mouse cDCs. We confirmed the reported in vitro requirement for in cDC1 development and the general role for in cDC development in competitive settings. However, deletion of did not abrogate the in vivo development of cDC1. Instead, deficiency caused only a selective reduction in CD8α expression by cDC1 without affecting XCR1 or CD24 expression. Normal cDC1 development was confirmed in mice by development of XCR1 -GFP cDC1 by rejection of syngeneic tumors and by priming of tumor-specific CD8 T cells. In summary, regulates a subset of cDC1-specific markers and is required in vitro but not in vivo for cDC1 development.
转录抑制剂 已被报道是一组称为 cDC1 的经典树突状细胞 (cDC) 发育所必需的,cDC1 负责交叉呈递。然而,其机制和体内功能分析一直缺乏。我们生成了一种条件性删除小鼠 cDC 中 的系统。我们证实了报告中 的体外 cDC1 发育要求和 的一般作用 在竞争环境中的 cDC 发育。然而, 删除并没有消除 cDC1 的体内发育。相反, 缺陷仅导致 cDC1 中 CD8α表达的选择性降低,而不影响 XCR1 或 CD24 的表达。通过排斥同种异体肿瘤和启动肿瘤特异性 CD8 T 细胞,在 小鼠中证实了正常的 cDC1 发育。总之, 调节一组 cDC1 特异性标记物,并且在体外需要,但在体内不需要 cDC1 的发育。