Abstract |
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 TH2 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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Authors | Caroline Aspord, Marie-Therese Leccia, Julie Charles, Joel Plumas |
Journal | Oncoimmunology
(Oncoimmunology)
Vol. 3
Issue 1
Pg. e27402
(Jan 01 2014)
ISSN: 2162-4011 [Print] United States |
PMID | 24701375
(Publication Type: Journal Article)
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