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本文引用的文献

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Trappin-2/Elafin: a novel innate anti-human immunodeficiency virus-1 molecule of the human female reproductive tract.Trappin-2/Elafin:一种新型的人生殖道天然抗人类免疫缺陷病毒-1 分子。
Immunology. 2010 Feb;129(2):207-19. doi: 10.1111/j.1365-2567.2009.03165.x. Epub 2009 Jul 18.
2
CCL20/MIP3alpha is a novel anti-HIV-1 molecule of the human female reproductive tract.CCL20/MIP3α是人类女性生殖道中的一种新型抗HIV-1分子。
Am J Reprod Immunol. 2009 Jul;62(1):60-71. doi: 10.1111/j.1600-0897.2009.00713.x.
3
Uterine DCs are crucial for decidua formation during embryo implantation in mice.子宫树突状细胞对小鼠胚胎植入过程中蜕膜的形成至关重要。
J Clin Invest. 2008 Dec;118(12):3954-65. doi: 10.1172/JCI36682. Epub 2008 Nov 20.
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Kinetics of murine decidual dendritic cells.小鼠蜕膜树突状细胞的动力学
Reproduction. 2007 Jan;133(1):275-83. doi: 10.1530/rep.1.01232.
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Innate immunity--cross-talk with adaptive immunity through pattern recognition receptors and cytokines.固有免疫——通过模式识别受体和细胞因子与适应性免疫相互作用。
Curr Opin Immunol. 2007 Feb;19(1):1-3. doi: 10.1016/j.coi.2006.11.018. Epub 2006 Dec 8.
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Analysis of endometrial myeloid and lymphoid dendritic cells during mouse estrous cycle.小鼠发情周期中子宫内膜髓样和淋巴样树突状细胞的分析
J Reprod Immunol. 2006 Aug;71(1):28-40. doi: 10.1016/j.jri.2006.01.003. Epub 2006 Jun 27.
7
Effect of oestradiol on PAMP-mediated CCL20/MIP-3 alpha production by mouse uterine epithelial cells in culture.雌二醇对培养的小鼠子宫上皮细胞中病原体相关分子模式介导的CCL20/巨噬细胞炎性蛋白-3α产生的影响。
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8
Effect of toll-like receptor (TLR) agonists on TLR and microbicide expression in uterine and vaginal tissues of the mouse.Toll样受体(TLR)激动剂对小鼠子宫和阴道组织中TLR及杀微生物剂表达的影响。
Am J Reprod Immunol. 2006 Jun;55(6):434-46. doi: 10.1111/j.1600-0897.2006.00381.x.
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Expression of Toll-like receptors (TLR) and responsiveness to TLR agonists by polarized mouse uterine epithelial cells in culture.培养的极化小鼠子宫上皮细胞中Toll样受体(TLR)的表达及对TLR激动剂的反应性
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Pathogen recognition and innate immunity.病原体识别与固有免疫
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角质细胞生长因子刺激小鼠子宫内膜上皮细胞分泌巨噬细胞炎性蛋白 3α 和角质细胞来源的趋化因子。

Keratinocyte Growth Factor Stimulates Macrophage Inflammatory Protein 3α and Keratinocyte-derived Chemokine Secretion by Mouse Uterine Epithelial Cells.

机构信息

Department of Physiology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA.

出版信息

Am J Reprod Immunol. 2010 Sep;64(3):197-211. doi: 10.1111/j.1600-0897.2010.00850.x.

DOI:10.1111/j.1600-0897.2010.00850.x
PMID:20455876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3837354/
Abstract

PROBLEM

communication between uterine epithelial cells and the underlying stromal fibroblasts is critical for proper endometrial function. Stromal fibroblast-derived growth factors have been shown to regulate epithelial immune functions. The purpose of this study was to determine whether keratinocyte growth factor (KGF) regulates uterine epithelial cell chemokine and antimicrobial secretion.

METHOD OF STUDY

uterine epithelial cells were isolated from Balb/c mice and cultured in either 96-well plates or transwell inserts. Epithelial cells were treated with KGF, epidermal growth factor (EGF), or hepatocyte growth factor (HGF). Macrophage inflammatory protein 3α (MIP3α) and keratinocyte-derived chemokine (KC) levels were measured by ELISA.

RESULTS

keratinocyte growth factor stimulated the secretion of MIP3α and KC. The effects on MIP3α by KGF were specific because EGF and HGF had no effect. In contrast, KGF, EGF, and HGF had similar effects on KC. Furthermore, KGF administered to the apical side of epithelial cells had no effect on MIP3α or KC secretion, indicating that the KGF receptor is located on the basolateral surface of uterine epithelial cells.

CONCLUSION

we demonstrate that KGF plays a role in uterine epithelial cell secretion of MIP3α and KC, key immune mediators involved in the protection of mucosal surfaces in the female reproductive tract.

摘要

问题

子宫上皮细胞与下方基质成纤维细胞之间的通讯对于子宫内膜的正常功能至关重要。已经表明基质成纤维细胞衍生的生长因子可调节上皮免疫功能。本研究的目的是确定角质细胞生长因子(KGF)是否调节子宫上皮细胞趋化因子和抗菌肽的分泌。

研究方法

从小鼠的子宫中分离出上皮细胞,并在 96 孔板或 Transwell 插入物中进行培养。用 KGF、表皮生长因子(EGF)或肝细胞生长因子(HGF)处理上皮细胞。通过 ELISA 测量巨噬细胞炎性蛋白 3α(MIP3α)和角质细胞衍生的趋化因子(KC)的水平。

结果

角质细胞生长因子刺激 MIP3α 和 KC 的分泌。KGF 对 MIP3α 的作用是特异性的,因为 EGF 和 HGF 没有作用。相比之下,KGF、EGF 和 HGF 对 KC 具有相似的作用。此外,在细胞的顶侧施加 KGF 对 MIP3α 或 KC 的分泌没有影响,这表明 KGF 受体位于子宫上皮细胞的基底外侧表面。

结论

我们证明 KGF 在子宫上皮细胞分泌 MIP3α 和 KC 中起作用,MIP3α 和 KC 是参与保护女性生殖道黏膜表面的关键免疫介质。