Several Treg-modulating and Treg-depleting strategies have been shown to reduce tumor burden and increase the antitumor immune response in both experimental models and the clinic. 5 6 Moreover, Tregs have been shown to hamper the efficacy of immunotherapy, 7 emphasizing the need for potent and specific ti-Treg targeting strategies. 3 4 This protumoral role of Tregs is corroborated by the finding that a high Foxp3 + Treg infiltration correlates with a poor prognosis in multiple cancer types. In the tumor microenvironment (TME), Tregs (tumor-infiltrating Tregs or ti-Tregs) have been shown to contribute to the suppression of antitumor immune responses and the development of an immunosuppressive TME in distinct cancer types. 1 Several mechanisms have been reported through which Tregs can mediate their suppressive function, including the release of immunosuppressive cytokines such as interleukin (IL)-10 and TGF-β (transforming growth factor-beta), the sequestering of IL-2 via the constitutive and high expression of CD25 and the cell-surface expression of immune checkpoint molecules such as CTLA-4, PD-1 and LAG-3. 1 They are characterized by the expression of the Foxp3 transcription factor, which is known to be a master regulator of Treg differentiation and suppressor function. Regulatory T cells (Tregs) are an immunosuppressive subset of T lymphocytes known to play a crucial role in immune homeostasis and self-tolerance.
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