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Estradiol regulates MICA expression in human endometrial cells.

机译:雌二醇调节人子宫内膜细胞中的MICA表达。

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摘要

The human endometrium undergoes cyclical changes regulated by sex hormones. Evidence suggests that sex hormones regulate NK cell recruitment into the uterus in large numbers. NKG2D is an activating receptor expressed on human NK cells, gammadelta and CD8 T cells. NKG2D ligands are known to be sensors of cellular stress expression of NKG2D ligands in the human uterus. Estradiol increased MICA expression on uterine epithelial cells; regulation was estrogen receptor-dependent. Real-time PCR analysis showed that NKG2D ligands MICA and MICB were expressed in the human endometrium. MICA protein was detected primarily on epithelial cells, and greater expression was observed in immunohistochemical analysis of tissues from patients in the secretory phase of the menstrual cycle. Thus, estrogens regulate expression of MICA. These data suggest hormonal regulation of innate immunity and NKG2D-mediated recognition in other tissues and diseases where estrogen may be involved.
机译:人的子宫内膜经历周期性变化,该变化由性激素调节。有证据表明,性激素可大量调节NK细胞向子宫的募集。 NKG2D是在人类NK细胞,γ和CD8 T细胞上表达的激活受体。已知NKG2D配体是人子宫中NKG2D配体的细胞应激表达的传感器。雌二醇增加子宫上皮细胞上MICA的表达;调节是雌激素受体依赖性的。实时PCR分析表明,NKG2D配体MICA和MICB在人子宫内膜中表达。主要在上皮细胞上检测到MICA蛋白,并且在月经周期分泌期的患者组织的免疫组织化学分析中观察到了更大的表达。因此,雌激素调节MICA的表达。这些数据表明在可能涉及雌激素的其他组织和疾病中,先天免疫的激素调节和NKG2D介导的识别。

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