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Peer-reviewedCC BY-NC 4.0Immunity & Inflammation

Disinhibiting dendritic cell-natural killer cell cooperation against metastasis

  • Oliver Kepp
  • Guido Kroemer
Open at sourcePDFDOICite

Abstract

Metastatic tumors evade not only adaptive but also innate immune control. In a recent paper published in China Science Life Sciences, Jin and colleagues identify EID1 as a transcriptional and functional brake shared by dendritic cells (DCs) and natural killer (NK) cells. Genetic or nanoparticle-mediated EID1 inhibition strengthens DC-NK apposition, augments FPR1-dependent type I and II interferon responses through a mechanism involving FPR1 and potentially NK cell-derived ANXA1, and suppresses experimental metastatic colonization/outgrowth. The work connects a transcriptional-corepressor to innate immunosurveillance and suggests that the previously described ANXA1-FPR1 danger-sensing module may operate not only between dying cancer cells and DCs in primary sites, but also among NK cells and DCs at metastatic lesions.

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Cite

BibTeXRIS
BibTeX
@article{kepp2026disinhibiting,
  title = {{Disinhibiting dendritic cell-natural killer cell cooperation against metastasis}},
  author = {Oliver Kepp and Guido Kroemer},
  journal = {Immunity \& Inflammation},
  year = {2026},
  month = sep,
  doi = {10.1007/s44466-026-00060-2},
  url = {https://hal.science/hal-05801093v1},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Disinhibiting dendritic cell-natural killer cell cooperation against metastasis
AU  - Oliver Kepp
AU  - Guido Kroemer
PY  - 2026
DA  - 2026/09/23
JO  - Immunity & Inflammation
DO  - 10.1007/s44466-026-00060-2
UR  - https://hal.science/hal-05801093v1
AB  - Metastatic tumors evade not only adaptive but also innate immune control. In a recent paper published in China Science Life Sciences, Jin and colleagues identify EID1 as a transcriptional and functional brake shared by dendritic cells (DCs) and natural killer (NK) cells. Genetic or nanoparticle-mediated EID1 inhibition strengthens DC-NK apposition, augments FPR1-dependent type I and II interferon responses through a mechanism involving FPR1 and potentially NK cell-derived ANXA1, and suppresses experimental metastatic colonization/outgrowth. The work connects a transcriptional-corepressor to innate immunosurveillance and suggests that the previously described ANXA1-FPR1 danger-sensing module may operate not only between dying cancer cells and DCs in primary sites, but also among NK cells and DCs at metastatic lesions.
SN  - 3059-4774
SN  - 3059-4774
ER  -