Regulatory T cell (CD4+CD25+ FOXP3+) (Treg cell)

Regulatory T cells (Tregs) are a specialized subset of CD4+ T cells characterized by high expression of CD25 (the α-chain of the IL-2 receptor), low CD127, and the lineage-defining transcription factor FOXP3[3][5][8]. They play a central role in maintaining immune homeostasis and self-tolerance by suppressing excessive or misdirected immune responses through cell contact–dependent and cytokine-mediated mechanisms (e.g., IL-10, TGF-β, IL-35 secretion)[2][7][8]. Tregs are broadly classified into natural (thymus-derived) and induced (peripherally generated); both types prevent autoimmunity and limit chronic inflammation[3][5][9]. Their immunosuppressive actions are mediated via direct inhibition of effector T cells, modulation of antigen-presenting cells, alteration of local metabolism, and negative feedback on cytokine availability (especially IL-2)[1][2][6][8]. In disease, Tregs are crucial for balancing immunity: for example, their depletion is associated with autoimmunity, whereas increased Treg frequency is linked to poor tumor immune surveillance and cancer progression[7][9]. Tregs are a prominent therapeutic target—efforts focus on manipulating their numbers or function to enhance anti-tumor immunity or combat autoimmune disorders. However, targeting Tregs requires care—loss of function leads to autoimmunity, while excess suppression can favor tumor or chronic infection[7][9]. Their identification relies primarily on FOXP3, CD4, and CD25 markers, but further specificity and selectivity are necessary for effective clinical application[3][8][9].

Other names

regulatory T cellTreg cellCD4+CD25+ regulatory T cellCD4+CD25+FOXP3+ T cellsuppressor T cellnatural Treg (nTreg)induced Treg (iTreg)CD4+ regulatory T cell

Depletion or inhibition of Treg cells to enhance anti-tumor immunity (anti-CD25, cyclophosphamide); Expansion of Treg cells for correction of autoimmunity (low-dose IL-2); Checkpoint blockade removes Treg-mediated immunosuppression (anti-CTLA-4); Modulation of metabolic signaling (e.g., via mTOR inhibitors, alters Treg/effector balance)