Paradoxic inhibition of human natural interferon-producing cells by the activating receptor NKp44

DOI PDF 4 Citations
  • Anja Fuchs
    From the Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO; and the Department of Clinical Research, Nagasaki Medical Center of Neurology, Nagasaki, Japan.
  • Marina Cella
    From the Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO; and the Department of Clinical Research, Nagasaki Medical Center of Neurology, Nagasaki, Japan.
  • Takayuki Kondo
    From the Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO; and the Department of Clinical Research, Nagasaki Medical Center of Neurology, Nagasaki, Japan.
  • Marco Colonna
    From the Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO; and the Department of Clinical Research, Nagasaki Medical Center of Neurology, Nagasaki, Japan.

Description

<jats:title>Abstract</jats:title> <jats:p>Natural killer (NK) cell-mediated cytotoxicity is triggered by multiple activating receptors associated with the signaling adaptor protein DNAX activation protein 12/killer cell-activating receptor-associated protein (DAP12/KARAP). Here, we show that one of these receptors, NKp44, is present on a subset of natural interferon-producing cells (IPCs) in tonsils. NKp44 expression can also be induced on blood IPCs after in vitro culture with interleukin 3 (IL-3). Crosslinking of NKp44 does not trigger IPC-mediated cytotoxicity but, paradoxically, inhibits interferon α (IFN-α) production by IPCs in response to cytosine-phosphate-guanosine (CpG) oligonucleotides. We find that IPCs in tonsils are in close contact with CD8+ T cells and demonstrate that a subset of memory CD8+ T cells produces IL-3. Therefore, IL-3-mediated induction of NKp44 on IPCs may be an important component of the ongoing crosstalk between the innate and adaptive immune response that allows memory CD8+ T cells to control the IPC response to virus. (Blood. 2005;106: 2076-2082)</jats:p>

Journal

  • Blood

    Blood 106 (6), 2076-2082, 2005-09-15

    American Society of Hematology

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