CD1d-restricted natural killer T (NKT) cells are potent immunoregulatory cells. Activation of invariant NKT (iNKT) cells suppresses tumor formation in murine models, and iNKT cells can naturally protect against spontaneous tumors and enhance immune responses to infections. Intestinal tumors develop in an environment of constant microbial pressure and inflammatory signals that enhance tumor formation. Notably, NKT cells promote murine inflammatory bowel disease, raising the question whether NKT cells would suppress or promote tumor formation in this tissue. Here we have investigated the role for NKT cells in intestinal tumor immunity using the APC^Min/+ mouse model for human colorectal cancer. APC^Min/+ mice develop intestinal polyps due to a mutation in the adenomatous polyposis coli (APC) gene, recapitulating early events in human colorectal cancerogenesis. The APC gene is mutated in 100% of familial and 80% of sporadic human colorectal cancer. Absence of iNKT cells in APC^Min/+ mice decreased the total number of intestinal polyps with 60%. iNKT cells were present in the polyps of APC^Min/+ mice, and showed a distinct phenotype compared to other organs, being CD4⁺, NK1.1^- CD44⁺, CD69⁺ and PD-1^lo, and had a predominant transcription factor expression of NKT1 cells. In APC^Min/+ Ja18^-/- mice, absence of iNKT cells was associated with a reduced frequency of Treg cells and lower expression levels of FoxP3 protein and transcript uniquely in the polyps. Moreover, in iNKT cell deficient APC^Min/+ mice, expression of TH1-associated genes, such as IFN-g and INOS, was increased in polyps, concomitant with elevated frequencies of conventional CD4⁺ and CD8⁺ T cells in this tissue. The results suggest that iNKT cells promote intestinal polyp formation by enhancing Treg cells and local immunosuppression of anti-tumor TH1-immunity.