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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Defective development of splenic and epidermal CD4(+) dendritic cells in mice deficient for IFN regulatory factor-2
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Defective development of splenic and epidermal CD4(+) dendritic cells in mice deficient for IFN regulatory factor-2

机译：小鼠脾脏和表皮CD4（+）树突状细胞发育缺陷IFN调节因子2缺陷

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Dendritic cells (DCs) play important roles in the initiation and regulation of immune responses. Although several subsets of DCs were identified according to their expression of surface molecules such as CD4, CD8, and CD11b, the regulatory mechanism for the development and homeostasis of these DC subsets remains unclear. Here we show that mice lacking IFN regulatory factor-2 (IRF-2(-/-) mice) exhibited a marked and selective defect in splenic CD4(+)CD11b(+)DCs, instead of CD8alpha(+)CD11b(-)DCs that were reported to be missing in mice lacking the related transcription factor IRF-8. Furthermore, the numbers of epidermal Langerhans cells in IRF2(-/-) mice were reduced at least in part because of the lack of the CD4(+)CD11b(+) subset. Studies with radiation bone marrow chimeras as well as in vitro retrovirus-mediated gene transduction showed that IRF-2 was required cell-autonomously for the development of myeloid-related DCs. Notably, these abnormalities in DCs diminished in mice lacking both IRF-2 and the IFN-alpha/beta receptor, indicating that IRF-2 acted through negatively regulating IFN-alpha/beta signals. In contrast, natural killer cells still showed developmental arrest in these double mutant mice, indicating that the mode of action of IRF-2 for CD4(+)DC development is distinct from that for natural killer cell development. Our current findings thus pointed to a previously unknown unique cell-type-selective multimode function of IRF-2 in the regulation of lymphohematopoiesis. [References: 39]
机译：树突状细胞（DC）在免疫反应的启动和调节中起重要作用。尽管根据DCs的表面分子（例如CD4，CD8和CD11b）的表达确定了DC的几个子集，但这些DC子集的发育和稳态的调节机制仍不清楚。在这里，我们显示缺少IFN调节因子2的小鼠（IRF-2（-/-）小鼠）脾脏CD4（+）CD11b（+）DCs而不是CD8alpha（+）CD11b（-）表现出明显的选择性缺陷。据报道，缺少相关转录因子IRF-8的小鼠缺少DC。此外，由于缺少CD4（+）CD11b（+）子集，IRF2（-/-）小鼠中表皮朗格汉斯细胞的数量至少有所减少。放射骨髓嵌合体以及体外逆转录病毒介导的基因转导研究表明，IRF-2是细胞自主产生髓样相关DC所必需的。值得注意的是，在缺乏IRF-2和IFN-α/β受体的小鼠中DC的这些异常现象减少了，这表明IRF-2通过负调节IFN-α/β信号发挥作用。相反，天然杀伤细胞在这些双重突变小鼠中仍显示出发育停滞，表明IRF-2对CD4（+）DC发育的作用方式不同于天然杀伤细胞的发育方式。因此，我们目前的发现指出了IRF-2在调节淋巴造血过程中独特的细胞类型选择性多模功能。 [参考：39]

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