Colorectal cancer is related to inflammatory bowel disease which is a chronic inflammatory state in the gastrointestinal tract. Gut macrophage expressing CX3CR1 plays an immunoregulatory role in the gut immune homeostasis. Aryl hydrocarbon receptor (AhR), a ligand-dependent endogenous receptor plays a role as a transcription factor to xenobiotic element which is considered as an environmental sensor. Although the roles of AhR in several immune cells such as T cells have been extensively exploited, their role in gut macrophages needs to be investigated. The objective of the study is to investigate the role of AhR in colon macrophages and furthermore in colorectal cancer. AhR deficiency on CX3CR1+ macrophages induces more infiltration of pro-inflammatory type macrophage into inflamed colon tissue. AhR deficient macrophage secreted enhanced chemokines such as CCL2, CCL7, CCL8, and CCL12 which are associated with monocyte infiltration. Interestingly, AhR deficient macrophages produced high level of IL-6 which is associated with tumor progression. Mice having AhR deficient macrophages increased the number of tumor nodules in AOM/DSS model. These results suggested that AhR in colon macrophages suppresses colorectal tumor promotion via conditioning an immune-regulatory gut environment.