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Title:
Regulatory T cells in tumor microenvironment: new mechanisms, potential therapeutic strategies and future prospects | Molecular Cancer
Description:
Regulatory T cells (Tregs) characterized by the expression of the master transcription factor forkhead box protein p3 (Foxp3) suppress anticancer immunity, thereby hindering protective immunosurveillance of tumours and hampering effective antitumour immune responses in tumour-bearing hosts, constitute a current research hotspot in the field. However, Tregs are also essential for the maintenance of the immune tolerance of the body and share many molecular signalling pathways with conventional T cells, including cytotoxic T cells, the primary mediators of tumour immunity. Hence, the inability to specifically target and neutralize Tregs in the tumour microenvironment without globally compromising self-tolerance poses a significant challenge. Here, we review recent advances in characterizing tumour-infiltrating Tregs with a focus on the functional roles of costimulatory and inhibitory receptors in Tregs, evaluate their potential as clinical targets, and systematically summarize their roles in potential treatment strategies. Also, we propose modalities to integrate our increasing knowledge on Tregs phenotype and function for the rational design of checkpoint inhibitor-based combination therapies. Finally, we propose possible treatment strategies that can be used to develop Treg-targeted therapies.
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Keywords {🔍}
tregs, pubmed, cells, article, google, scholar, cas, regulatory, central, cell, cancer, function, foxp, expression, tumour, immune, immunol, effector, immunity, suppressive, treg, activation, tumours, depletion, human, ctla, wang, antitumour, signalling, nat, activity, res, tcell, mice, zhang, transcription, enhanced, blockade, receptor, antictla, tumor, immunotherapy, control, ifnγ, liu, differentiation, development, patients, treatment, metabolism,
Topics {✒️}
foxo1/cebpb/nf-κb/ccl20 axis fc-region–modified anti-ctla-4 mab anti-cd3/cd28/cd2-induced proliferation foxo1/cebpb/nf-kappab signaling peroxisome proliferator-activated receptor-beta fc-engineered anti-ctla-4 antibody foxo1/cebpb/nf-κb signalling pi3k/akt/foxo1/3 signalling cascade antibody-dependent macrophage-mediated depletion de-fucosylated anti-ccr4 antibody irae-prone anti-ctla-4 mab nf-kappab c-rel amplify il-2r-stat5 signaling excessive th2-type-dominant responses article download pdf isoform-specific inhibitor effective long-lived central tregs tumor-specific treg-targeted antibodies cancer cell-derived il-1α pro-autophagy protein ambra1 fatty acid-binding proteins anti-pd-1/pd-l1 therapy [178] cell-driven hev neogenesis gr-1+cd11b+ myeloid cells ph-sensitive anti-ctla-4 antibodies treg-specific demethylated region serine-threonine kinase mst1 activated β-catenin signature mtorc1-hif-1α axis transcription factors t-bet activates latent tgf-β enterotoxigenic bacteroides fragilis cell-derived interferon-gamma form stat3-foxp3 complexes ti-tregs produce ifn-γ single-cell rna-sequencing anti-tim-3-treated mice showed malt1 protease-dependent manner il-2-fc fusion proteins treg-expressing ctla-4 combines adult t-cell leukemia k-akt-mtorc1 signalling tumor-infiltrating human cd4 hif-1α bound directly tumour-producing chemokine ccl17 tumour antigen-selective manner anti-ctla-4 antibody treatment tgf-β-dependent manner combining treg-targeting therapies tlr8 signalling-mediated reprogramming
Questions {❓}
- Do suppressor T cells exist?
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WebPage:
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headline:Regulatory T cells in tumor microenvironment: new mechanisms, potential therapeutic strategies and future prospects
description:Regulatory T cells (Tregs) characterized by the expression of the master transcription factor forkhead box protein p3 (Foxp3) suppress anticancer immunity, thereby hindering protective immunosurveillance of tumours and hampering effective antitumour immune responses in tumour-bearing hosts, constitute a current research hotspot in the field. However, Tregs are also essential for the maintenance of the immune tolerance of the body and share many molecular signalling pathways with conventional T cells, including cytotoxic T cells, the primary mediators of tumour immunity. Hence, the inability to specifically target and neutralize Tregs in the tumour microenvironment without globally compromising self-tolerance poses a significant challenge. Here, we review recent advances in characterizing tumour-infiltrating Tregs with a focus on the functional roles of costimulatory and inhibitory receptors in Tregs, evaluate their potential as clinical targets, and systematically summarize their roles in potential treatment strategies. Also, we propose modalities to integrate our increasing knowledge on Tregs phenotype and function for the rational design of checkpoint inhibitor-based combination therapies. Finally, we propose possible treatment strategies that can be used to develop Treg-targeted therapies.
datePublished:2020-07-17T00:00:00Z
dateModified:2020-07-17T00:00:00Z
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headline:Regulatory T cells in tumor microenvironment: new mechanisms, potential therapeutic strategies and future prospects
description:Regulatory T cells (Tregs) characterized by the expression of the master transcription factor forkhead box protein p3 (Foxp3) suppress anticancer immunity, thereby hindering protective immunosurveillance of tumours and hampering effective antitumour immune responses in tumour-bearing hosts, constitute a current research hotspot in the field. However, Tregs are also essential for the maintenance of the immune tolerance of the body and share many molecular signalling pathways with conventional T cells, including cytotoxic T cells, the primary mediators of tumour immunity. Hence, the inability to specifically target and neutralize Tregs in the tumour microenvironment without globally compromising self-tolerance poses a significant challenge. Here, we review recent advances in characterizing tumour-infiltrating Tregs with a focus on the functional roles of costimulatory and inhibitory receptors in Tregs, evaluate their potential as clinical targets, and systematically summarize their roles in potential treatment strategies. Also, we propose modalities to integrate our increasing knowledge on Tregs phenotype and function for the rational design of checkpoint inhibitor-based combination therapies. Finally, we propose possible treatment strategies that can be used to develop Treg-targeted therapies.
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