Abstract
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.