Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Shanghai Medical College of Fudan University, Shanghai 200011, China.
Cell Mol Immunol. 2010 Jan;7(1):51-60. doi: 10.1038/cmi.2009.102.
The chemokine thymus-expressed chemokine (TECK), which regulates T-cell development and tissue-specific homing, has been identified as a potential contributor to the pathogenesis and progression of endometriosis. Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD), an air pollutant, and estrogen also appear to be involved in endometriosis. Both endometrial stromal cells (ESCs) and the combination of 17beta-estradiol and TCDD increase the secretion of TECK in the endometriosis-associated cells and promote the invasiveness of ESCs by increasing expression of matrix metalloproteinase (MMP)-2 and MMP-9. Anti-TECK neutralizing antibodies can effectively inhibit the invasiveness of ESCs and the expression of MMP-2 and MMP-9 in the cells. Interestingly, the expression of chemokine C receptor 9 (CCR9) and its ligand TECK increases significantly in the endometriotic milieu of patients with endometriosis. Therefore, the over-expressed TECK interacts with CCR9 on the ESCs in the endometriotic milieu, which may contribute to the onset and progression of endometriosis.
趋化因子胸腺表达趋化因子（TECK），它调节 T 细胞的发育和组织特异性归巢，已被确定为子宫内膜异位症发病机制和进展的潜在贡献者。二恶英（2,3,7,8-四氯二苯并对二恶英，TCDD），一种空气污染物，和雌激素也似乎参与子宫内膜异位症。子宫内膜基质细胞（ESCs）和 17β-雌二醇和 TCDD 的组合增加了与子宫内膜异位症相关的细胞中 TECK 的分泌，并通过增加基质金属蛋白酶（MMP）-2 和 MMP-9 的表达促进 ESCs 的侵袭性。抗 TECK 中和抗体可有效抑制 ESCs 的侵袭性以及细胞中 MMP-2 和 MMP-9 的表达。有趣的是，趋化因子 C 受体 9（CCR9）及其配体 TECK 在子宫内膜异位症患者的子宫内膜异位症环境中表达显著增加。因此，过度表达的 TECK 与子宫内膜异位症环境中的 ESCs 上的 CCR9 相互作用，这可能有助于子宫内膜异位症的发生和进展。
