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Human regulatory T cells (Tregs) are a specialized subpopulation of T cells that act as a 'brake' on the immune system, ensuring that immune responses do not become overactive or attack the body's own tissues, a process known as self-tolerance (Sakaguchi et al., 2008, Cell). They are classically defined by the expression of the transcription factor FOXP3 and high levels of the interleukin-2 receptor alpha chain (CD25), which are essential for their development and suppressive function (Fontenot et al., 2003, Nature Immunology). In clinical practice, Tregs are therapeutic targets in two opposing ways: in autoimmune diseases and transplantation, drugs like low-dose IL-2 (Aldesleukin) are used to expand Treg populations to restore tolerance (Klatzmann & Abbas, 2015, Nature Reviews Immunology). In oncology, however, Tregs often infiltrate tumors and protect them from the immune system, leading to the development of therapies like Ipilimumab or Mogamulizumab that aim to deplete or inhibit these cells to boost anti-tumor immunity (Togashi et al., 2019, Nature Reviews Clinical Oncology). The label 'specific molecular target unknown' suggests that while the therapeutic effect is mediated through the Treg cell population, the precise molecular trigger or binding site may be undefined or part of a complex cellular therapy. This designation is often used in early-stage drug discovery or for phenotypic screening hits where the cellular effect is clear but the exact protein interactor remains to be identified.
Modulation of regulatory T cell frequency, stability, or suppressive function to alter immune homeostasis.
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