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

doi:10.1126/science.285.5428.727

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Science 30 July 1999:
Vol. 285. no. 5428, pp. 727 - 729
DOI: 10.1126/science.285.5428.727

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Reports

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

Stefan Bauer, ¹^* Veronika Groh, ¹^* Jun Wu, ² Alexander Steinle, ¹ Joseph H. Phillips, ² Lewis L. Lanier, ² Thomas Spies ¹

Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for $gamma$ $delta$ T cells and is frequently expressed in epithelial tumors. A receptorfor MICA was detected on most $gamma$ $delta$ T cells, CD8⁺ $alpha$ $beta$ T cells, and natural killer (NK) cells and was identifiedas NKG2D. Effector cells from all these subsets could be stimulatedby ligation of NKG2D. Engagement of NKG2D activated cytolyticresponses of $gamma$ $delta$ T cells and NK cells against transfectants andepithelial tumor cells expressing MICA. These results define anactivating immunoreceptor-MHC ligand interaction that may promoteantitumor NK and T cell responses.

¹ Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
² DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304, USA.
^*   These authors contributed equally to this work and are listed in alphabetical order.

   Present address: Technical University of Munich, Institute of Microbiology, Trogerstrasse 32, D-81675 Munich, Germany.

   To whom correspondence should be addressed. E-mail: tspies{at}fred.fhcrc.org