Published online Oct 28, 2012. doi: 10.3748/wjg.v18.i40.5688
Revised: April 6, 2012
Accepted: April 12, 2012
Published online: October 28, 2012
Regulatory T cells (Tregs) are key elements in immunological self-tolerance. The number of Tregs may alter in both peripheral blood and in colonic mucosa during pathological circumstances. The local cellular, microbiological and cytokine milieu affect immunophenotype and function of Tregs. Forkhead box P3+ Tregs function shows altered properties in inflammatory bowel diseases (IBDs). This alteration of Tregs function can furthermore be observed between Crohn’s disease and ulcerative colitis, which may have both clinical and therapeutical consequences. Chronic mucosal inflammation may also influence Tregs function, which together with the intestinal bacterial flora seem to have a supporting role in colitis-associated colorectal carcinogenesis. Tregs have a crucial role in the immunoevasion of cancer cells in sporadic colorectal cancer. Furthermore, their number and phenotype correlate closely with the clinical outcome of the disease, even if their contribution to carcinogenesis has previously been controversial. Despite knowledge of the clinical relationship between IBD and colitis-associated colon cancer, and the growing number of immunological aspects encompassing sporadic colorectal carcinogenesis, the molecular and cellular links amongst Tregs, regulation of the inflammation, and cancer development are still not well understood. In this paper, we aimed to review the current data surrounding the role of Tregs in the pathogenesis of IBD, colitis-associated colon cancer and sporadic colorectal cancer.