Tregceller

Regulatory T cells, or Tregs, are a specialized subset of CD4+ T lymphocytes that suppress immune responses and maintain self-tolerance. They help prevent autoimmunity, limit collateral tissue damage during inflammation, and promote tolerance to commensals and transplanted tissue. Human and mouse Tregs share expression of the transcription factor FOXP3, which is essential for their development and function. They characteristically express high levels of CD25 (the IL-2 receptor α chain) and reduced CD127 (IL-7 receptor α chain); CTLA-4 is commonly expressed and marks suppressive activity.

Most Tregs develop in the thymus (thymus-derived Tregs, tTregs), whereas additional regulatory cells can arise in the periphery from conventional CD4+ T cells under TGF-β and IL-2 signaling (peripheral or induced Tregs, iTregs). FOXP3 expression stabilizes the regulatory lineage and is associated with epigenetic changes, including demethylation of the FOXP3 TSDR; iTregs often show more variable FOXP3 stability. Tregs exert suppression through multiple mechanisms: consumption of IL-2, secretion of inhibitory cytokines such as IL-10 and TGF-β (and sometimes IL-35), expression of CTLA-4 to modulate antigen-presenting cells, and, in some contexts, direct cytolysis or metabolic disruption of effector cells.

Clinical relevance of Tregs includes protection against autoimmune disease and promotion of transplant tolerance. Dysregulation or deficiency of Tregs contributes to autoimmune disorders; in cancer, elevated Treg activity can hinder anti-tumor immunity. Therapeutic approaches under investigation include expansion or adoptive transfer of Tregs, as well as strategies to modulate their function or stability in vivo.