Imbalance of T cell regulation can be sufficient on its own to initiate or propagate autoimmunity in various chronic inflammatory diseases such as inflammatory bowel disease (IBD) or rheumatoid arthritis. In line with this concept, recent transgenic animal models highlight the role of T cell regulation in the development of autoimmune diseases. For instance, IL-2 receptor −/− mice were shown to develop severe anemia and IBD [161] , possibly due to the decreased numbers of Tregs facilitating autoimmune reactivity in the presence of proliferating (and probably, activated) T-cells. Absence of the IL-2 receptor in these animals leads to proliferation of T cells and decreased numbers of Tregs.