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.

Human ovarian cyclic function is a complex process. Ovarian failure can lead to a loss of not only female hormonal function, which depends on cyclic changes of gonadotropin levels, but to the absence of oocytes. Whereas there are numerous factors associated with ovarian dysfunction and de- creased female fertility, the autoimmune mechanisms have been put forward by several investigators. In ovarian pathology, such as idiopathic infertility, premature ovarian failure and polycystic ovarian syndrome, immunological etiology has been suggested.