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The regulatory T cells (Tregs), formerly known as suppressor T cells, are a subpopulation of T cells which modulate the immune system, maintain tolerance to self-antigens, and abrogate autoimmune disease. These cells generally suppress or downregulate induction and proliferation of effector T cells. Additional regulatory T cells known as Treg17 cells have recently been identified.

Tregs express CD4, FoxP3, and CD24 and are thought to be derived from the same lineage as naïve CD4 cells. Because effector T cells also express CD4 and CD25, Tregs are very difficult to effectively differentiate, making them difficult to study.

Mouse models have suggested that modulation of Tregs can treat autoimmune disease and cancer, and facilitate organ transplantation. The implication that they have for cancer are complicated., Tregs tend to be up-regulated in individuals with cancer and they seem to be recruited to the cite of many tumors. Studies in both humans and animal models have implicated that high levels of Tregs in tumor environment is indicative of a poor prognosis, and Tregs are thought to suppress tumor immunity, thus hindering the body's innate ability to control the growth of cancerous cells. Recent immunotherapy research is studying how regulation of T cells could possibly be utilized in the treatment of cancer.

Most tumors elicit an immune response in the host that is mediated by tumor antigens, thus distinguishing the tumor from other non-cancerous cells. This is evidenced by the large number of, tumor-infiltrating lymphocytes (TIL) which are often found in the tumor microenvironment. Theoretically, these lymphocytes target cancerous cells and therefore slow or terminate the development of the tumor. However, this process is complicated because Tregs seem to be preferentially trafficked to the tumor microenvironment. While Tregs normally make only about 4% of CD4+ T Cells, they can make up as much as 20-30% of the total CD4+ population around the tumor microenvironment.

Although high levels of TIL was initially thought to be important in determining an immune response against cancer, it is now widely recognized that the ratio of Tregs to Teffectors  in the tumor microenvironment is a  determining factor in the success the immune response against the cancer. High levels of Tregs in the tumor microenvironment are associated with poor prognosis in many cancers, such as ovarian, breast, renal, and pancreatic cancer. This indicates that Tregs suppress Teffector cells and hinder the body's immune response against the cancer. However, in some types of cancer the opposite is true--and high levels of Tregs are associated with a positive prognosis. This trend is seen in cancers such as colorectal carcinoma  and follicular lymphoma. This could be due to Treg's ability to suppress general inflammation which is known to trigger cell proliferation and metastasis. These opposite effects indicate that Treg's role in the development of cancer is highly dependent on both type and location of cancer.

Although it is still not entirely understood how Tregs are preferentially trafficked to the tumor microenvironment, the chemotaxis is probably driven by the production of chemokines by the tumor. Treg infiltration into the tumor microenvironment is facilitated by the binding of the chemokine receptor CCR4, which is expressed on Tregs, to its ligand CCL22, which is secreted by many types of tumor cells. Treg expansion at the cite of the tumor could also explain the increased levels of Tregs. The cytokine, TGF-β, which is commonly produced by tumor cells, is known to induce the expansion of Tregs.

In general the immunosuppression of the tumor microenvironment has largely contributed to the unsuccessful outcomes of many cancer immunotherapy treatments. Depletion of Tregs in animal models had shown an increased efficacy of immunotherapy treatments, and therefore, many immunotherapy treatments are now incorporating Treg depletion.