Abnormal regulation of chemokine TECK and its receptor CCR9 in the endometriotic milieu is involved in pathogenesis of endometriosis by way of enhancing invasiveness of endometrial stromal cells

作者：Wang, Yun; Yu, Jing; Luo, Xuezhen; Wang, Xiaoqiu; Li, Mingqing; Wang, Ling; Li, Dajin^*

来源：Cellular and Molecular Immunology, 2010, 7(1): 51-60.

DOI：10.1038/cmi.2009.102

• TECK
• CCR9
• DSC
• invasiveness
• endometriosis

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 17 beta-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. Cellular & Molecular Immunology (2010) 7, 51-60; doi:10.1038/cmi.2009.102

• 出版日期2010-1
• 单位海南医学院; 复旦大学