Significance of regulatory T cells in cancer immunology and immunotherapy

Abstract

Understanding the cross-talk between cancer cells and immune cells in the tumour microenvironment (TME) is a key issue in cancer immunity. The interaction between cancer cells and the immune system during cancer development is summarized as the "cancer immunoediting" hypothesis, consisting of elimination, equilibrium, and escape phases. 1 In particular, immunosuppressive mechanisms by immunosuppressive cells, including regulatory T (Treg) cells, are established for unrestrained tumour growth in the escape phase. While Treg cells are essential for maintaining immune homeostasis, such as immune tolerance against self-antigens, they also play a central role in suppressing antitumor immune responses in cancer immunity. Thus, Treg cell depletion augments the efficacy of cancer immunotherapy by disrupting the immunosuppressive state. 2 Despite preclinical and clinical experiments on the efficacy of Treg cell-targeted therapy,Treg cell depletion-induced autoimmune diseases are concerned. 3,4 Treg cell depletion results in the loss of not only tumour infiltrating

Chimeric antigen receptor T cells in the treatment of osteosarcoma (Review)

“…As Tregs have high-affinity IL-2 receptors but produce minimal IL-2 themselves, this leads to a lack of IL-2 for effector T cells, resulting in their dysfunction. Lastly, Tregs secrete immunosuppressive cytokines like IL-10 and IL-35, directly inhibiting the activation of T cells ( 119 ).…”

Deciphering Regulatory T-Cell Dynamics in Cancer Immunotherapy: Mechanisms, Implications, and Therapeutic Innovations

“…Contrary to effector and memory T lymphocytes, Tregs have a greater ability to identify most of the tumor-associated antigens that are produced when tumor cells die. This triggers their activation and multiplication, hence strengthening the immunosuppressive characteristics of the TME . In addition, Tregs express the inducible T-cell costimulatory molecule ICOS, which belongs to the CTLA-4/PD-1/CD28 .…”

“…This triggers their activation and multiplication, hence strengthening the immunosuppressive characteristics of the TME. 39 In addition, Tregs express the inducible T-cell costimulatory molecule ICOS, which belongs to the CTLA-4/PD-1/CD28. 40 It facilitates their activation and multiplication by interacting with the ICOS ligand found on plasmacytoid DCs.…”

Natural Killer Cells Reprogram Myeloid-Derived Suppressor Cells to Induce TNF-α Release via NKG2D–Ligand Interaction after Cryo-Thermal Therapy

“…Immunotherapies such as the PD-1/PD-L1 immune checkpoint blockade, which is widely used in clinical practice, focus on enhancing T cell activity [1]; however, the complexity of the tumor microenvironment (TME) limits the response. The unsatisfactory efficacy of immunotherapy is partially due to the role of immunosuppressive myeloid cells in the suppression of anti-tumor immunity [2,3]. Myeloid-derived suppressor cells (MDSCs) are a community of immature myeloid cells (IMCs) that can potently suppress immune cell effector functions during tumor progression [4].…”