Abstract
Treg play a central role in maintenance of self tolerance and homeostasis through suppression of self-reactive T cell populations. In addition to that role, Treg also survey cancers and suppress anti-tumor immune responses. Thus, understanding the unique attributes of Treg-tumor interactions may permit control of this pathologic suppression without interfering with homeostatic self-tolerance. This review will define the unique role of Treg in cancer growth, and the ways by which Treg inhibit a robust anti-tumor immune response. There will be specific focus placed on Treg homing to the tumor microenvironment (TME), TME formation of induced Treg (iTreg), mechanisms of suppression that underpin cancer immune escape, and trophic nonimmunologic effects of Treg on tumor cells.
Highlights
Natural T Regulatory Cells (Treg), induced by self-antigens in the thymus, home to sites of tumors, while induced Treg (iTreg), induced by antigens in the periphery, are created as a result of a specific cytokine milieu of the tumor microenvironment (TME)
Tregs are a subset of CD4+ T cells that are distinguished from immune cells through expression of Forkhead box protein 3 (FoxP3) transcription factor
CD4+CD25+ FoxP3+ Natural Treg (nTreg) and iTreg express characteristic receptors including cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), Treg and the Suppressive Tumor Microenvironment glucocorticoid-induced TNFR-related gene (GITR), and CD25 (IL-2 receptor α-chain) which further differentiate from other immune cells, and which mediate immunosuppressive functions [10, 11]
Summary
Natural Treg (nTreg), induced by self-antigens in the thymus, home to sites of tumors, while iTreg, induced by antigens in the periphery, are created as a result of a specific cytokine milieu of the TME. CD4+CD25+ FoxP3+ nTreg and iTreg express characteristic receptors including cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), Treg and the Suppressive Tumor Microenvironment glucocorticoid-induced TNFR-related gene (GITR), and CD25 (IL-2 receptor α-chain) which further differentiate from other immune cells, and which mediate immunosuppressive functions [10, 11].
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