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Melanoma hijacks plasmacytoid dendritic cells to promote its own progression

Despite their elevated immunogenicity, melanoma lesions often escape immunosurveillance. We have recently demonstrated that plasmacytoid dendritic cells (pDCs) accumulating within melanomas are prompted to express tumor necrosis factor (ligand) superfamily, member 4 (TNFSF4, best known as OX40L) and...

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Detalles Bibliográficos
Autores principales: Aspord, Caroline, Leccia, Marie-Therese, Charles, Julie, Plumas, Joel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962506/
https://www.ncbi.nlm.nih.gov/pubmed/24701375
http://dx.doi.org/10.4161/onci.27402
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author Aspord, Caroline
Leccia, Marie-Therese
Charles, Julie
Plumas, Joel
author_facet Aspord, Caroline
Leccia, Marie-Therese
Charles, Julie
Plumas, Joel
author_sort Aspord, Caroline
collection PubMed
description Despite their elevated immunogenicity, melanoma lesions often escape immunosurveillance. We have recently demonstrated that plasmacytoid dendritic cells (pDCs) accumulating within melanomas are prompted to express tumor necrosis factor (ligand) superfamily, member 4 (TNFSF4, best known as OX40L) and inducible T-cell co-stimulator ligand (ICOSL), hence becoming able to trigger T(H)2 and regulatory immune responses. Such a hijacking of pDCs is associated with early disease relapse. Thus, by actively harnessing the plasticity of pDCs, melanomas promote their own progression.
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spelling pubmed-39625062014-04-03 Melanoma hijacks plasmacytoid dendritic cells to promote its own progression Aspord, Caroline Leccia, Marie-Therese Charles, Julie Plumas, Joel Oncoimmunology Author's View Despite their elevated immunogenicity, melanoma lesions often escape immunosurveillance. We have recently demonstrated that plasmacytoid dendritic cells (pDCs) accumulating within melanomas are prompted to express tumor necrosis factor (ligand) superfamily, member 4 (TNFSF4, best known as OX40L) and inducible T-cell co-stimulator ligand (ICOSL), hence becoming able to trigger T(H)2 and regulatory immune responses. Such a hijacking of pDCs is associated with early disease relapse. Thus, by actively harnessing the plasticity of pDCs, melanomas promote their own progression. Landes Bioscience 2014-01-01 /pmc/articles/PMC3962506/ /pubmed/24701375 http://dx.doi.org/10.4161/onci.27402 Text en Copyright © 2014 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Author's View
Aspord, Caroline
Leccia, Marie-Therese
Charles, Julie
Plumas, Joel
Melanoma hijacks plasmacytoid dendritic cells to promote its own progression
title Melanoma hijacks plasmacytoid dendritic cells to promote its own progression
title_full Melanoma hijacks plasmacytoid dendritic cells to promote its own progression
title_fullStr Melanoma hijacks plasmacytoid dendritic cells to promote its own progression
title_full_unstemmed Melanoma hijacks plasmacytoid dendritic cells to promote its own progression
title_short Melanoma hijacks plasmacytoid dendritic cells to promote its own progression
title_sort melanoma hijacks plasmacytoid dendritic cells to promote its own progression
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962506/
https://www.ncbi.nlm.nih.gov/pubmed/24701375
http://dx.doi.org/10.4161/onci.27402
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