Cutting edge: The AP-1 subunit JunB determines NK cell-mediated target cell killing by regulation of the NKG2D-ligand RAE-1ε

Norman Nausch, Lore Florin, Bettina Hartenstein, Peter Angel, Marina Schorpp-Kistner, Adelheid Cerwenka

    Research output: Contribution to journalArticle

    35 Scopus citations

    Abstract

    The activating receptor NKG2D and its ligands RAE-1 play an important role in the NK, γδ+, and CD8+ T cell-mediated immune response to tumors. Expression levels of RAE-1 on target cells have to be tightly controlled to allow immune cell activation against tumors but to avoid destruction of healthy tissues. In this study, we report that cell surface expression of RAE-1ε is greatly enhanced on cells lacking JunB, a subunit of the transcription complex AP-1. Furthermore, tissue-specific junB knockout mice respond to 12-O-tetradecanoyl-phorbol-13-acetate, a potent AP-1 activator, with markedly increased and sustained epidermal RAE-1ε expression. Accordingly, junB-deficient cells are efficiently killed via NKG2D by NK cells and induce IFN-γ production. Our data indicate that the transcription factor AP-1, which is involved in tumorigenesis and cellular stress responses, regulates RAE-1ε. Thus, up-regulated RAE-1ε expression due to low levels of JunB could alert immune cells to tumors and stressed cells.

    Original languageEnglish (US)
    Pages (from-to)7-11
    Number of pages5
    JournalJournal of Immunology
    Volume176
    Issue number1
    DOIs
    StatePublished - Jan 1 2006

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Immunology

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