OBJECTIVES Endometriosis (EMS) is a benign disease that is related to estrogen, immune disorders and inflammation. The purpose of this research was to determine the expression of CD200 in EMS and to clarify its role in the pathogenesis of the disease. METHODS The levels of serum CD200 in patients with and without EMS were determined by ELISA. Furthermore, the expression of CD200 in normal eutopic endometrium and ectopic endometrium was detected by immunohistochemistry and western blotting. The CD200 receptor (CD200R) in macrophages in peritoneal fluid (pMØ) obtained from controls and patients with EMS was examined by western blotting. CD200 expression in human endometrial stromal cells (HESCs) stimulated with 17β-estradiol (E2) was measured by western blotting. Furthermore, macrophages were stimulated with different concentrations of CD200 and the effect on phagocytosis was analyzed. RESULTS The plasma CD200 levels of patients with EMS was significantly increased compared with controls (P = 0.0173, 95%CI [18.75, 159.6]). Compared with normal eutopic endometrium, the expression of CD200 was significantly increased in ectopic endometrial tissues. The CD200R expression in pMØ obtained from patients with EMS was increased compared with the controls (P = 0.0244). CD200 expression in HESCs stimulated with E2 was up-regulated. As the levels of CD200 increased, macrophage phagocytosis in vitro gradually decreased. CONCLUSIONS CD200 is an estrogen-induced molecule that impairs macrophage phagocytosis and may contribute to the immune escape of ectopic lesions in EMS.

中文翻译：

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雌激素调节的CD200抑制子宫内膜异位症中的巨噬细胞吞噬作用。

目的子宫内膜异位症（EMS）是一种与雌激素，免疫疾病和炎症有关的良性疾病。这项研究的目的是确定CD200在EMS中的表达，并阐明其在疾病发病机理中的作用。方法采用ELISA法测定有无EMS患者的血清CD200水平。此外，通过免疫组织化学和western blotting检测CD200在正常异位子宫内膜和异位子宫内膜中的表达。通过蛋白质印迹法检查从对照组和EMS患者获得的腹膜液（pMØ）巨噬细胞中的CD200受体（CD200R）。通过蛋白质印迹法测量在用17β-雌二醇（E2）刺激的人子宫内膜基质细胞（HESCs）中的CD200表达。此外，用不同浓度的CD200刺激巨噬细胞，并分析其对吞噬作用的影响。结果与对照组相比，EMS患者的血浆CD200水平显着增加（P = 0.0173，95％CI [18.75，159.6]）。与正常的异位子宫内膜相比，异位子宫内膜组织中CD200的表达明显增加。与对照组相比，从EMS患者获得的pMØ中CD200R表达增加（P = 0.0244）。E2刺激的HESC中CD200的表达上调。随着CD200水平的增加，体外巨噬细胞的吞噬作用逐渐降低。结论CD200是雌激素诱导的分子，可损害巨噬细胞的吞噬作用，并可能有助于EMS中异位病变的免疫逃逸。结果与对照组相比，EMS患者的血浆CD200水平显着增加（P = 0.0173，95％CI [18.75，159.6]）。与正常的异位子宫内膜相比，异位子宫内膜组织中CD200的表达明显增加。与对照组相比，从EMS患者获得的pMØ中CD200R表达增加（P = 0.0244）。E2刺激的HESC中CD200的表达上调。随着CD200水平的增加，体外巨噬细胞的吞噬作用逐渐降低。结论CD200是雌激素诱导的分子，可损害巨噬细胞的吞噬作用，并可能有助于EMS中异位病变的免疫逃逸。结果与对照组相比，EMS患者的血浆CD200水平显着增加（P = 0.0173，95％CI [18.75，159.6]）。与正常异位子宫内膜相比，异位子宫内膜组织中CD200的表达明显增加。与对照组相比，从EMS患者获得的pMØ中CD200R表达增加（P = 0.0244）。E2刺激的HESC中CD200的表达上调。随着CD200水平的增加，体外巨噬细胞的吞噬作用逐渐降低。结论CD200是雌激素诱导的分子，可损害巨噬细胞的吞噬作用，并可能有助于EMS中异位病变的免疫逃逸。CD200在异位子宫内膜组织中的表达明显增加。与对照组相比，从EMS患者获得的pMØ中CD200R表达增加（P = 0.0244）。E2刺激的HESC中CD200的表达上调。随着CD200水平的增加，体外巨噬细胞的吞噬作用逐渐降低。结论CD200是雌激素诱导的分子，可损害巨噬细胞的吞噬作用，并可能有助于EMS中异位病变的免疫逃逸。CD200在异位子宫内膜组织中的表达明显增加。与对照组相比，从EMS患者获得的pMØ中CD200R表达增加（P = 0.0244）。E2刺激的HESC中CD200的表达上调。随着CD200水平的增加，体外巨噬细胞的吞噬作用逐渐降低。结论CD200是雌激素诱导的分子，可损害巨噬细胞的吞噬作用，并可能有助于EMS中异位病变的免疫逃逸。