{"title":"Disinhibiting dendritic cell-natural killer cell cooperation against metastasis.","authors":"Oliver Kepp, Guido Kroemer","doi":"10.1007/s44466-026-00060-2","DOIUrl":null,"url":null,"abstract":"<p><p>Metastatic tumors evade not only adaptive but also innate immune control. In a recent paper published in <i>China Science Life Sciences</i>, 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.</p>","PeriodicalId":521105,"journal":{"name":"Immunity & inflammation","volume":"2 1","pages":"41"},"PeriodicalIF":0.0000,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13601072/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunity & inflammation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s44466-026-00060-2","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/9/23 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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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