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CD4-positive CD25-positive regulatory T cells, commonly known as Tregs, are a specialized subpopulation of T lymphocytes essential for maintaining immune homeostasis and preventing autoimmunity [1, 41]. They are defined by the constitutive expression of the interleukin-2 receptor alpha chain (CD25) and the master transcription factor FOXP3 [4, 15]. Tregs exert their suppressive effects through multiple mechanisms, including the secretion of anti-inflammatory cytokines like IL-10 and TGF-beta, the consumption of IL-2 to starve effector T cells, and direct cell-to-cell contact-mediated inhibition [9, 13]. In oncology, Tregs often infiltrate the tumor microenvironment and suppress anti-tumor immunity, making them a target for depletion or functional blockade to improve the efficacy of cancer treatments [5, 11]. Conversely, in autoimmune diseases and organ transplantation, therapeutic strategies focus on expanding the Treg population or using adoptive cell transfer to restore self-tolerance and prevent graft rejection [8, 42]. This entry describes a cell population rather than a single molecular target, although specific surface receptors on these cells are often the direct targets of pharmacological intervention [11, 18].
Therapeutic strategies targeting these cells involve the depletion of regulatory T cells to enhance anti-tumor immunity, the expansion of regulatory T cells to restore immune tolerance in autoimmune diseases, the inhibition of their suppressive function, or the adoptive transfer of ex vivo expanded or engineered regulatory T cells [11, 13, 42].
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