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Boshuizen, Julia; Vredevoogd, David W; Krijgsman, Oscar; Ligtenberg, Maarten A; Blankenstein, Stephanie; de Bruijn, Beaunelle; Frederick, Dennie T; Kenski, Juliana C N; Parren, Mara; Brüggemann, Marieke; Madu, Max F; Rozeman, Elisa A; Song, Ji-Ying; Horlings, Hugo M; Blank, Christian U; van Akkooi, Alexander C J; Flaherty, Keith T; Boland, Genevieve M; Peeper, Daniel S
Nature communications, 08/2020, Letnik: 11, Številka: 1Journal Article
Melanomas can switch to a dedifferentiated cell state upon exposure to cytotoxic T cells. However, it is unclear whether such tumor cells pre-exist in patients and whether they can be resensitized to immunotherapy. Here, we chronically expose (patient-derived) melanoma cell lines to differentiation antigen-specific cytotoxic T cells and observe strong enrichment of a pre-existing NGFR population. These fractions are refractory also to T cells recognizing non-differentiation antigens, as well as to BRAF + MEK inhibitors. NGFR cells induce the neurotrophic factor BDNF, which contributes to T cell resistance, as does NGFR. In melanoma patients, a tumor-intrinsic NGFR signature predicts anti-PD-1 therapy resistance, and NGFR tumor fractions are associated with immune exclusion. Lastly, pharmacologic NGFR inhibition restores tumor sensitivity to T cell attack in vitro and in melanoma xenografts. These findings demonstrate the existence of a stable and pre-existing NGFR multitherapy-refractory melanoma subpopulation, which ought to be eliminated to revert intrinsic resistance to immunotherapeutic intervention.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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