As an anti-implantation contraception medicine, mifepristone can alter the development of the endometrium. In contrast, little research is performed to decipher the effect of mifepristone on Th1/Th2 immune homeostasis in the endometrium. CD14⁺ monocytes derived from healthy donors are cultured with interleukin (IL)-4 and granulocyte macrophage-colony stimulating factor to induce monocyte-derived dendritic cells (DCs), which are further incubated with mifepristone. Mifepristone incubation could induce up-regulated CD83 and major histocompatibility complex cell surface receptor staining on monocyte-derived DCs. Functionally, mifepristone incubation could enhance the allostimulatory capacity of DCs to promote the proliferation of allogeneic T cells with up-regulated Th1 cell proportion and down-regulated Th2 cell proportion. On the other side, increased Th1 cytokines release (interferon-γ, tumor necrosis factor α), inhibited Th2 cytokines release (IL-10, IL-4), promoted T-Box transcription factor 21 transcription, and inhibited GATA binding protein 3 transcription are also identified. Mifepristone-stimulated DCs could alter the Th1/Th2 transcription balance to favor Th1 skewing inflammatory environment.

中文翻译：

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米非司酮通过诱导单核细胞来源的树突状细胞成熟来调节 Th1/Th2 的极化

作为一种抗着床避孕药，米非司酮可以改变子宫内膜的发育。相比之下，很少有研究来解释米非司酮对子宫内膜 Th1/Th2 免疫稳态的影响。来自健康供体的 CD14 + 单核细胞与白细胞介素 (IL)-4 和粒细胞巨噬细胞集落刺激因子一起培养，以诱导单核细胞衍生的树突状细胞 (DC)，并进一步与米非司酮一起孵育^。米非司酮孵育可诱导单核细胞来源的 DC 上 CD83 和主要组织相容性复合物细胞表面受体染色上调。从功能上讲，米非司酮孵育可增强DC的同种刺激能力，促进同种异体T细胞增殖，上调Th1细胞比例，下调Th2细胞比例。另一方面，增加Th1细胞因子释放（干扰素-γ、肿瘤坏死因子α），抑制Th2细胞因子释放（IL-10、IL-4），促进T-Box转录因子21转录，抑制GATA结合蛋白3转录也被识别出来。米非司酮刺激的 DC 可以改变 Th1/Th2 转录平衡，以有利于 Th1 倾斜的炎症环境。