Immune cells infiltrate tumors and make up a significant component of the multicellular cancer microenvironment, yet the immune system often fails to prevent tumor formation and progression. One explanation for this paradox is the presence of tolerance-promoting regulatory T cells (Tregs). Tregs were known to be essential for maintaining self-tolerance. Tregs have been found to promote tolerance to tumors in mouse models. Treg infiltration in human tumors and malignant ascites is associated with worse clinical outcomes for various types of cancers.

Many studies that took place after discovery of regulatory T (Treg) cells have widened our, still incomplete, knowledge about that specialized cell population. Treg cells differentiate mainly in the thymus, but this process occurs also in the periphery. They suppress proliferation of other cells (CD4, CD8, B lymphocytes, NK) in direct, cell to cell, interactions in vitro and therefore are main controllers of the proper immune response. Deficiency as well as functional dysregulation of this population may be responsible for development of autoimmune events.

The mechanism that plays an essential role in immunosuppression and regulation is the presence of naturally arising CD4+CD25+ T lymphocytes (Treg). Quantitative or qualitative dysfunc- tions in these cells may lead to autoimmune diseases. The Foxp3, a forkhead/winged helix (FKH) trans- cription factor, is the key regulatory gene for the development and function of regulatory T lymphocytes. The Foxp3 expression is limited to CD4+CD25+ T cells at both mRNA and protein levels. The Foxp3 interacts with nuclear factor of activated T cells (NFAT) and repress cytokine gene expression.

Recent studies have underscored the importance of regulatory T cells (Treg) in the maintenance of immunological self-tolerance and in the prevention of autoimmune diseases. Regulatory T cells is heterogenic subpopulation of T cells, that is able to suppress functions of effector cells during the immune response. Among them are natural (CD4+CD25+) and induced Treg (Tr1, Th3, CD4+CD25-) that gain their unique fenotype during the development in the thymus or in the periphery, respectively.