CCL25 (TECK) binds to CCR9, the only known receptor for TECK. CCR9 is expressed by a small population of circulating memory CD4+ and CD8+ lymphocytes expressing the intestinal homing receptor alpha4beta7. Therefore, CCL25 is a key regulator for CCR9+CD4+ alpha4beta7 T cell homing to the small intestine. In addition, CCL25 induces adhesion ofCD103+ (alphaEbeta7) on CD8 intraepithelial lymphocytes to its epithelial ligand E-cadherin. In inflammatory bowel diseases (IBD), as in celiac and Crohn’s diseases, the proportion of CCR9+ cells in the peripheral blood and in the gut seems to be inversed; there is a lower frequency of CCR9+CD4+ T cells in the gut mucosa than in the peripheral blood. Also, a decrease in CCR9+CD4+ T cells occurs in the gut of HIV-infected patients. This decrease correlates with a lower expression of CCL25 by inflamed gut endothelial cells. Unusual expression of CCL25 in the liver occurs in primary sclerosis cholangitis (extra-intestinal complication of IBD). In this way, human T cells activated in the gut can be recruited to liver endothelium. Functional expression of CCR9 has been detected in melanoma derived cells, and it has been associated to small intestine metastatic melanoma processes. In addition, CCR9 is expressed by ovarian, breast, and prostate cancer cells.