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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
Descripción
Sumario: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.