Regulatory T (Treg) cells, which suppress self-reactive immune responses, also inhibit anti-tumor immunity by infiltrating tumors. Their presence is often linked to poor prognosis. Removing Treg cells can enhance anti-tumor immunity but may cause autoimmunity. Targeting specific Treg subsets, like effector Treg cells, is a promising strategy to avoid autoimmunity. Effector Treg cells express molecules like CCR4 and CTLA-4, which can be targeted with monoclonal antibodies. Anti-CTLA-4 antibodies, for example, can deplete effector Treg cells or reduce their suppressive activity. Combining Treg-targeting with cancer vaccines or immune checkpoint inhibitors could improve cancer immunotherapy. Treg cells maintain self-tolerance by suppressing immune responses, but their depletion can enhance tumor-specific T cell activation. Treg cells in tumors are often effector Treg cells, which are highly proliferative and express high levels of CTLA-4. Targeting these cells with antibodies like anti-CCR4 can selectively deplete them, enhancing anti-tumor immunity. Other approaches include using agonistic antibodies against Treg-specific molecules like GITR or small molecules that target Treg signaling pathways. While Treg depletion can improve cancer immunotherapy, it must be carefully managed to avoid autoimmunity. Understanding Treg heterogeneity and function is crucial for developing effective and safe therapies. Current research focuses on targeting specific Treg subsets to enhance anti-tumor responses without causing severe autoimmunity.Regulatory T (Treg) cells, which suppress self-reactive immune responses, also inhibit anti-tumor immunity by infiltrating tumors. Their presence is often linked to poor prognosis. Removing Treg cells can enhance anti-tumor immunity but may cause autoimmunity. Targeting specific Treg subsets, like effector Treg cells, is a promising strategy to avoid autoimmunity. Effector Treg cells express molecules like CCR4 and CTLA-4, which can be targeted with monoclonal antibodies. Anti-CTLA-4 antibodies, for example, can deplete effector Treg cells or reduce their suppressive activity. Combining Treg-targeting with cancer vaccines or immune checkpoint inhibitors could improve cancer immunotherapy. Treg cells maintain self-tolerance by suppressing immune responses, but their depletion can enhance tumor-specific T cell activation. Treg cells in tumors are often effector Treg cells, which are highly proliferative and express high levels of CTLA-4. Targeting these cells with antibodies like anti-CCR4 can selectively deplete them, enhancing anti-tumor immunity. Other approaches include using agonistic antibodies against Treg-specific molecules like GITR or small molecules that target Treg signaling pathways. While Treg depletion can improve cancer immunotherapy, it must be carefully managed to avoid autoimmunity. Understanding Treg heterogeneity and function is crucial for developing effective and safe therapies. Current research focuses on targeting specific Treg subsets to enhance anti-tumor responses without causing severe autoimmunity.