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首页> 外文期刊>EMBO Journal >Id2 expression delineates differential checkpoints in the genetic program of CD8alpha+ and CD103+ dendritic cell lineages.
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Id2 expression delineates differential checkpoints in the genetic program of CD8alpha+ and CD103+ dendritic cell lineages.

机译：Id2表达要表达的微分检查点的遗传程序CD8alpha +和CD103 +树突细胞谱系。

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摘要

Dendritic cells (DCs) have critical roles in the induction of the adaptive immune response. The transcription factors Id2, Batf3 and Irf-8 are required for many aspects of murine DC differentiation including development of CD8alpha(+) and CD103(+) DCs. How they regulate DC subset specification is not completely understood. Using an Id2-GFP reporter system, we show that Id2 is broadly expressed in all cDC subsets with the highest expression in CD103(+) and CD8alpha(+) lineages. Notably, CD103(+) DCs were the only DC able to constitutively cross-present cell-associated antigens in vitro. Irf-8 deficiency affected loss of development of virtually all conventional DCs (cDCs) while Batf3 deficiency resulted in the development of Sirp-alpha(-) DCs that had impaired survival. Exposure to GM-CSF during differentiation induced expression of CD103 in Id2-GFP(+) DCs. It did not restore cross-presenting capacity to Batf3(-/-) or CD103(-)Sirp-alpha(-)DCs in vitro. Thus, Irf-8 and Batf3 regulate distinct stages in DC differentiation during the development of cDCs. Genetic mapping DC subset differentiation using Id2-GFP may have broad implications in understanding the interplay of DC subsets during protective and pathological immune responses.
机译：树突状细胞(dc)的关键角色诱导的适应性免疫反应。转录因子Id2, Batf3 Irf-8所需的许多方面鼠分化包括发展CD8alpha(+)和CD103 DCs(+)。直流子集规范并不完全理解。在所有疾病预防控制中心显示Id2广泛表达最高的子集表达CD103 (+)和CD8alpha(+)血统。只有直流能持续吗cross-present细胞相关抗原体外。Irf-8不足影响发展的损失几乎所有传统的DCs(疾控中心),而Batf3缺陷导致的发展sirpα(-)DCs受损的生存。暴露在gm - csf在分化诱导表达式的CD103 Id2-GFP DCs(+)。恢复cross-presenting Batf3能力(- / -)或CD103 (-) sirpα(-)DCs体外。和Batf3调节不同的阶段分化在疾病预防控制中心的发展。遗传分化使用映射直流子集Id2-GFP可能有广泛的影响理解直流子集的相互作用保护和病理性免疫反应。

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