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    NK cells stimulate recruitment of cDC1 into the tumor microenvironment promoting cancer immune control.

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    Authors
    Böttcher, J
    Bonavita, Eduardo
    Chakravarty, P
    Blees, H
    Cabeza-Cabrerizo, M
    Sammicheli, S
    Rogers, N
    Sahai, E
    Zelenay, Santiago
    Reis E Sousa, C
    Affiliation
    Immunobiology Laboratory, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
    Issue Date
    2018-02-22
    
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    Abstract
    Conventional type 1 dendritic cells (cDC1) are critical for antitumor immunity, and their abundance within tumors is associated with immune-mediated rejection and the success of immunotherapy. Here, we show that cDC1 accumulation in mouse tumors often depends on natural killer (NK) cells that produce the cDC1 chemoattractants CCL5 and XCL1. Similarly, in human cancers, intratumoral CCL5, XCL1, and XCL2 transcripts closely correlate with gene signatures of both NK cells and cDC1 and are associated with increased overall patient survival. Notably, tumor production of prostaglandin E2 (PGE2) leads to evasion of the NK cell-cDC1 axis in part by impairing NK cell viability and chemokine production, as well as by causing downregulation of chemokine receptor expression in cDC1. Our findings reveal a cellular and molecular checkpoint for intratumoral cDC1 recruitment that is targeted by tumor-derived PGE2for immune evasion and that could be exploited for cancer therapy.
    Citation
    NK cells stimulate recruitment of cDC1 into the tumor microenvironment promoting cancer immune control. 2018, 172(5):1022-1037.e14 Cell
    Journal
    Cell
    URI
    http://hdl.handle.net/10541/620834
    DOI
    10.1016/j.cell.2018.01.004
    PubMed ID
    29429633
    Type
    Article
    Language
    en
    ISSN
    1097-4172
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.cell.2018.01.004
    Scopus Count
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    All Paterson Institute for Cancer Research

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