Regulatory T (Treg) cells are essential for maintaining peripheral tolerance, preventing autoimmune diseases, and limiting chronic inflammatory diseases. However, they also suppress beneficial immune responses by inhibiting sterilizing immunity and anti-tumor immunity. This review discusses the mechanisms by which Treg cells mediate suppression and whether these mechanisms are crucial for their function. It also proposes that effector T cells may play a role in enhancing Treg function. Treg cells use several sophisticated mechanisms to maintain immune homeostasis, prevent autoimmunity, and moderate inflammation. These include suppression by inhibitory cytokines (such as IL-10 and TGFβ), suppression by cytolysis, suppression by metabolic disruption, and suppression by modulation of dendritic cell (DC) maturation or function. IL-10 and TGFβ are key mediators of Treg function, but their exact role in natural Treg cells remains debated. TGFβ is also important for the development of induced Treg cells. Treg cells can also suppress effector T cells through cytolysis, using granzymes and perforin. They can suppress effector T cells by inducing apoptosis through the TRAIL-DR5 pathway or by modulating DC maturation. Treg cells can also suppress effector T cells by metabolic disruption, such as through adenosine production, which inhibits effector T-cell function and promotes the generation of adaptive Treg cells. Treg cells can also suppress effector T cells by modulating the function of other cell types, such as DCs, monocytes, and macrophages. They can influence immune responses by modulating the recruitment and function of other cell types, such as mast cells. The mechanisms by which Treg cells suppress effector T cells are complex and context-dependent. While some mechanisms are contact-dependent, others may be more effective in different settings. The relative importance of Treg cell-derived IL-10 varies depending on the target organism or disease. The review also discusses the hypothesis that effector T cells may play an active role in enhancing Treg function. This is supported by recent findings showing that the presence of effector T cells can enhance the expression of IL-35 in Treg cells, which is crucial for their suppressive activity. Overall, the review highlights the complexity of Treg cell function and the need for further research to determine the relative importance of different mechanisms in various disease settings. The role of Treg cells in immune regulation is critical for maintaining immune homeostasis and preventing autoimmune diseases.Regulatory T (Treg) cells are essential for maintaining peripheral tolerance, preventing autoimmune diseases, and limiting chronic inflammatory diseases. However, they also suppress beneficial immune responses by inhibiting sterilizing immunity and anti-tumor immunity. This review discusses the mechanisms by which Treg cells mediate suppression and whether these mechanisms are crucial for their function. It also proposes that effector T cells may play a role in enhancing Treg function. Treg cells use several sophisticated mechanisms to maintain immune homeostasis, prevent autoimmunity, and moderate inflammation. These include suppression by inhibitory cytokines (such as IL-10 and TGFβ), suppression by cytolysis, suppression by metabolic disruption, and suppression by modulation of dendritic cell (DC) maturation or function. IL-10 and TGFβ are key mediators of Treg function, but their exact role in natural Treg cells remains debated. TGFβ is also important for the development of induced Treg cells. Treg cells can also suppress effector T cells through cytolysis, using granzymes and perforin. They can suppress effector T cells by inducing apoptosis through the TRAIL-DR5 pathway or by modulating DC maturation. Treg cells can also suppress effector T cells by metabolic disruption, such as through adenosine production, which inhibits effector T-cell function and promotes the generation of adaptive Treg cells. Treg cells can also suppress effector T cells by modulating the function of other cell types, such as DCs, monocytes, and macrophages. They can influence immune responses by modulating the recruitment and function of other cell types, such as mast cells. The mechanisms by which Treg cells suppress effector T cells are complex and context-dependent. While some mechanisms are contact-dependent, others may be more effective in different settings. The relative importance of Treg cell-derived IL-10 varies depending on the target organism or disease. The review also discusses the hypothesis that effector T cells may play an active role in enhancing Treg function. This is supported by recent findings showing that the presence of effector T cells can enhance the expression of IL-35 in Treg cells, which is crucial for their suppressive activity. Overall, the review highlights the complexity of Treg cell function and the need for further research to determine the relative importance of different mechanisms in various disease settings. The role of Treg cells in immune regulation is critical for maintaining immune homeostasis and preventing autoimmune diseases.