Activation of NK Cells and T Cells by NKG2D, a Receptor for Stress-Inducible MICA

  • Stefan Bauer
    Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
  • Veronika Groh
    Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
  • Jun Wu
    DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304, USA.
  • Alexander Steinle
    Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
  • Joseph H. Phillips
    DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304, USA.
  • Lewis L. Lanier
    DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304, USA.
  • Thomas Spies
    Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.

書誌事項

公開日
1999-07-30
DOI
  • 10.1126/science.285.5428.727
公開者
American Association for the Advancement of Science (AAAS)

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説明

<jats:p> Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for γδ T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most γδ T cells, CD8 <jats:sup>+</jats:sup> αβ T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of γδ T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses. </jats:p>

収録刊行物

  • Science

    Science 285 (5428), 727-729, 1999-07-30

    American Association for the Advancement of Science (AAAS)

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