Age-related deviations of the immune system contribute to a higher likelihood of infections, cancer, and autoimmunity in the elderly. Senescence of T-lymphocytes is characterized by phenotypical and functional changes including the loss of characteristic T-cell surface markers, while an increase of stimulatory receptors, cytotoxicity as well as resistance against apoptosis is observed. One of the key mediators of immune regulation are naturally occurring regulatory T-cells (T_regs). T_regs express high levels of CD25 and the intracellular protein forkhead box P3; they exert their suppressive functions in contact-dependent as well as contact-independent manners. Quantitative and qualitative defects of T_regs were observed in patients with autoimmune diseases. Increased T_reg activity was shown to suppress anti-tumor and anti-infection immunity. The effect of aging on T_regs, and the possible contribution of age-related changes of the T_reg pool to the pathophysiology of diseases in the elderly are still poorly understood. T_reg homeostasis depends on an intact thymic function and current data suggest that conversion of non-regulatory T-cells into T_regs as well as peripheral expansion of existing T_regs compensates for thymic involution after puberty to maintain constant T_reg numbers. In the conventional T-cell subset, peripheral proliferation of T-cells is associated with replicative senescence leading to phenotypical and functional changes. For T_regs, different developmental stages were also described; however, replicative senescence of T_regs has not been observed yet.