Mouse CCL28 was identified in an EST database using a human chemokine consensus sequence. CCL28 is constitutively expressed by mucosal epithelial cells such as exocrine glands, trachea, and colon. Acinar epithelial cells in human and mouse salivary glands are strongly positive for CCL28 by immunostaining, and human saliva and milk contain high concentrations of CCL28. Furthermore, it is known that human and mouse CCL28 have antimicrobial activity against Candida albicans, Gram-negative bacteria, and Gram-positive bacteria, and the the C terminus of human CCL28 is responsible for this property. In addition, using a CCR10 deficient mouse model, it was shown that CCR10 plays a critical role in localization and accumulation of IgA ASC to the lactating mammary gland. Also, it has been described that CCL28 is upregulated in epithelial inflammation and this upregulation allows the recruitment of T regs expressing CCR10. In fact, a subpopulation of CCR10-expressing CD25+CD4+Foxp3+ Tregs with potent anti-inflammatory properties was isolated from chronically inflamed human liver. Most recent information suggested that tumour hypoxia promotes the recruitment of Treg cells through induction of expression of CCL28, and this induction is mediated by the hypoxia inducible factor-1α (HIF-1α). Therefore, tumour hypoxia promotes tolerance and angiogenesis via CCL28 and Treg cells.