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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