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 attributed to the C-terminus of CCL28 against Candida albicans, Gram-negative bacteria, and Gram-positive bacteria. In addition, using a CCR10 deficient mouse model, it was shown that CCR10 plays a critical role in localization and accumulation of IgA ASC in lactating mammary glands. Also, it has been described that CCL28 is upregulated in epithelial inflammation, and this upregulation allows the recruitment of Tregs expressing CCR10. In fact, a subpopulation of CCR10-expressing CD25+ CD4+ FOXP3+ Tregs with potent anti-inflammatory properties was isolated from a chronically inflamed human liver. Information suggests that tumor hypoxia promotes the recruitment of Treg cells through induction of expression of CCL28, and this induction is mediated by the hypoxia inducible factor-1 alpha (HIF-1α). Therefore, tumor hypoxia promotes tolerance and angiogenesis via CCL28 and Tregs.