I clinical trial. Additionally, while regulatory T cells have been shown to increase via polyclonal expansion both systemically and locally during healthy pregnancies to protect the fetus from the maternal immune response (a process called maternal immune tolerance), there is evidence that this polyclonal expansion is impaired in preeclamptic mothers and their offspring. Research suggests reduced production and development of regulatory T cells during preeclampsia may degrade maternal immune tolerance, leading to the hyperactive immune response characteristic of preeclampsia. 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 causes large numbers of tumor-infiltrating lymphocytes (TILs) to be found in the tumor microenvironment. Although it is not entirely understood, it is thought that these lymphocytes target cancerous cells and therefore slow or terminate the development of the tumor. However, this process is complicated because Treg cells seem to be preferentially trafficked to the tumor microenvironment. While Treg cells normally make up 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 TILs were initially thought to be important in determining an immune response against cancer, it is now widely recognized that the ratio of Treg to effector T cells in the tumor microenvironment is a determining factor in the success of the immune response against the cancer. High levels of Treg cells in the tumor microenvironment are associated with poor prognosis in many cancers, such as ovarian, breast, renal, and pancreatic cancer. This indicates that Treg cells suppress effector T 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 Treg cells 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 cells' ability to suppress general inflammation which is known to trigger cell proliferation and metastasis . These opposite effects indicate that Treg cells' role in the development of cancer is highly dependent on both type and location of the tumor. Although it is still not entirely understood how Treg cells 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