Ccr6, a G protein-coupled receptor, is unique as it binds only to the chemokine ligand CCL20 [2,4]. It is expressed on various immune cells such as B cells, immature dendritic cells, innate lymphoid cells, regulatory CD4 T cells, and Th17 cells [1]. The CCR6-CCL20 axis is involved in leukocyte migration, immune homeostasis, and activation, playing a crucial role in mucosal immunity, for example, mediating the recruitment of immune cells to epithelial inflammation sites [1,2,4].

In colitis-associated carcinoma, SMAD4 loss in mouse colon epithelium led to increased CCL20 expression and recruitment of CCR6+ immune cells like T regulatory, Th17, and dendritic cells. Deletion of the Ccr6 gene abrogated these immune responses and significantly reduced the incidence of colitis-associated tumors, indicating that Ccr6 contributes to colon cancer susceptibility through CCL20-mediated inflammation [3].

In conclusion, Ccr6 is essential in immune-related biological processes, especially in mucosal immunity and immune cell recruitment. Gene knockout studies in mice, such as the Ccr6 deletion in the context of SMAD4-related colitis-associated carcinoma, have revealed its role in disease-related inflammation and carcinogenesis, highlighting its potential as a therapeutic target in related diseases.