Results
| PMID | 20081876 |
| Gene Name | CCL25 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Associated genes | CCR9, TECK |
| Other associated phenotypes |
Endometriosis |
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Cell Mol Immunol. 2010 Jan;7(1):51-60. doi: 10.1038/cmi.2009.102. Wang, Yun| Yu, Jing| Luo, Xuezhen| Wang, Xiaoqiu| Li, Mingqing| Wang, Ling| Li, Dajin Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Shanghai Medical College of Fudan University, Shanghai 200011, China. 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. Mesh Terms: Adult| Cell Line, Tumor| *Cell Movement| Cells, Cultured| Chemokines, CC/*immunology| Coculture Techniques| Endometriosis/genetics/*immunology| Estradiol/metabolism| Female| Humans| Matrix Metalloproteinase 2/biosynthesis| Matrix Metalloprotein |
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