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 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.
University Joseph Fourier; INSERM, U823; Immunobiology & Immunotherapy of Cancers; Grenoble, France ; French Blood Service; Rhone-Alpes; R&D-Laboratory; Grenoble, France.
Caroline
C
Aspord
University Joseph Fourier; INSERM, U823; Immunobiology & Immunotherapy of Cancers; Grenoble, France ; Dermatology Department; Grenoble University Hospital; Grenoble, France.
Marie-Therese
MT
Leccia
University Joseph Fourier; INSERM, U823; Immunobiology & Immunotherapy of Cancers; Grenoble, France ; Dermatology Department; Grenoble University Hospital; Grenoble, France.
Julie
J
Charles
University Joseph Fourier; INSERM, U823; Immunobiology & Immunotherapy of Cancers; Grenoble, France ; French Blood Service; Rhone-Alpes; R&D-Laboratory; Grenoble, France.
Joel
J
Plumas
ICOSL; OX40L; TH2; humanized mice; immune escape; melanoma; plasmacytoid dendritic cells; tumor microenvironment