4.6 Editorial Material

Melanoma hijacks plasmacytoid dendritic cells to promote its own progression

Journal

ONCOIMMUNOLOGY
Volume 3, Issue 1, Pages -

Publisher

LANDES BIOSCIENCE
DOI: 10.4161/onci.27402

Keywords

humanized mice; ICOSL; immune escape; melanoma; OX40L; plasmacytoid dendritic cells; T(H)2; tumor microenvironment

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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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