CCL28 is a C-C motif chemokine that functions as a key mucosal immune regulator and tumor microenvironment modulator. Primarily, CCL28 recruits CCR10+ IgA plasmablasts to mucosal tissues, particularly the lactating mammary gland and airway submucosal glands, where gland epithelial cells express CCL28 to support IgA plasma cell longevity and antibody secretion 1. In addition to mucosal immunity, CCL28 plays significant roles in tumor immunology. The chemokine recruits regulatory T cells (Treg) through the CCR10-CCL28 axis, contributing to immunosuppression in the tumor microenvironment 2. In colorectal cancer, the CCL28-CCR10 axis facilitates IgG plasma cell migration to tumor stroma and is implicated in immunosuppressive responses 3. CCL28 expression is upregulated through canonical WNT signaling in cancer stem cells 4 and through the β-catenin/CCL28 axis activated by bile acid signaling, leading to elevated intratumoral Treg infiltration and enhanced colorectal cancer progression under high-fat diet conditions 5. In liver metastases, CCL28 mediates recruitment of IgA+ plasma cells that promote immunosuppression 6. These findings suggest CCL28 blockade represents a potential therapeutic strategy to reprogram immunosuppressive tumor microenvironments.