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Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy

Tumors promote immune suppression and dendritic cells (DCs) play a key role in this. However, signaling networks that program DCs to induce immune suppression are unknown. In our recent study, we showed that tumors activate β-catenin/TCF4 in DCs programming them to a regulatory state, which promotes...

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Detalles Bibliográficos
Autores principales: Suryawanshi, Amol, Manicassamy, Santhakumar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635893/
https://www.ncbi.nlm.nih.gov/pubmed/26587326
http://dx.doi.org/10.1080/2162402X.2015.1052932
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author Suryawanshi, Amol
Manicassamy, Santhakumar
author_facet Suryawanshi, Amol
Manicassamy, Santhakumar
author_sort Suryawanshi, Amol
collection PubMed
description Tumors promote immune suppression and dendritic cells (DCs) play a key role in this. However, signaling networks that program DCs to induce immune suppression are unknown. In our recent study, we showed that tumors activate β-catenin/TCF4 in DCs programming them to a regulatory state, which promotes T regulatory responses while suppresses effector T cell responses. Thus, targeting DCs-β-catenin pathway represents a promising target for anticancer immunotherapy.
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spelling pubmed-46358932016-02-03 Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy Suryawanshi, Amol Manicassamy, Santhakumar Oncoimmunology Author's View Tumors promote immune suppression and dendritic cells (DCs) play a key role in this. However, signaling networks that program DCs to induce immune suppression are unknown. In our recent study, we showed that tumors activate β-catenin/TCF4 in DCs programming them to a regulatory state, which promotes T regulatory responses while suppresses effector T cell responses. Thus, targeting DCs-β-catenin pathway represents a promising target for anticancer immunotherapy. Taylor & Francis 2015-06-26 /pmc/articles/PMC4635893/ /pubmed/26587326 http://dx.doi.org/10.1080/2162402X.2015.1052932 Text en © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Author's View
Suryawanshi, Amol
Manicassamy, Santhakumar
Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy
title Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy
title_full Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy
title_fullStr Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy
title_full_unstemmed Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy
title_short Tumors induce immune tolerance through activation of β-catenin/TCF4 signaling in dendritic cells: A novel therapeutic target for cancer immunotherapy
title_sort tumors induce immune tolerance through activation of β-catenin/tcf4 signaling in dendritic cells: a novel therapeutic target for cancer immunotherapy
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635893/
https://www.ncbi.nlm.nih.gov/pubmed/26587326
http://dx.doi.org/10.1080/2162402X.2015.1052932
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