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¹ Molecular and Cell Based Discovery, ² Protein Biochemistry, ³ Bioinformatics, and ⁴ Autoimmunity and Inflammation, ZymoGenetics Inc., Seattle, WA 98102
⁵ Centre d'Immunologie de Marseille-Luminy, Université de la Méditerranée, Campus de Luminy, Marseille 13288, France
⁶ Institut National de la Santé et de la Recherche Médicale UMR 631, Marseille 13288, France
⁷ Centre National de la Recherche Scientifique UMR6102, Marseille 13288, France
⁸ Institut Paoli-Calmettes, Centre de Ressources Biologiques en Oncologie, Marseille 13009, France
⁹ Centre de Recherches en Cancérologie de Marseille, Institut National de la Santé et de la Recherche Médicale UMR 891, Marseille 13009, France
¹⁰ Dipartimento di Medicina Sperimentale e Centro di Eccellenza per le Ricerche Biomediche, Università degli Studi di Genova, Genova 16132, Italy
¹¹ Hôpital de la Conception, Assistance Publique - Hôpitaux de Marseille, Marseille 13005, France

CORRESPONDENCE Steven D. Levin: levins{at}zgi.com OR Eric Vivier: vivier{at}ciml.univ-mrs.fr

Cancer development is often associated with the lack of specific and efficient recognition of tumor cells by the immune system. Natural killer (NK) cells are lymphocytes of the innate immune system that participate in the elimination of tumors. We report the identification of a tumor cell surface molecule that binds NKp30, a human receptor which triggers antitumor NK cell cytotoxicity and cytokine secretion. This previously unannotated gene belongs to the B7 family and, hence, was designated B7-H6. B7-H6 triggers NKp30-mediated activation of human NK cells. B7-H6 was not detected in normal human tissues but was expressed on human tumor cells, emphasizing that the expression of stress-induced self-molecules associated with cell transformation serves as a mode of cell recognition in innate immunity.

© 2009 Brandt et al.
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