Disinhibiting dendritic cell-natural killer cell cooperation against metastasis.

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.