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Coengagement of CD16 and CD94 Receptors Mediates Secretion of Chemokines and Induces Apoptotic Death of Naive Natural Killer Cells

Authors' Affiliations: ¹ The Jane and Jerry Weintraub Center for Reconstructive Biotechnology and Division of Oral Biology and Medicine, Jonsson Comprehensive Cancer Center; Departments of ² Radiation Oncology and ³ Head and Neck Surgery, School of Dentistry and Medicine, University of California at Los Angeles, Los Angeles, California

Requests for reprints: Anahid Jewett, Division of Oral Biology and Medicine, University of California at Los Angeles School of Dentistry, 10833 Le Conte Avenue, Los Angeles, CA 90095-1668. Phone: 310-206-3970; Fax: 310-794-7109; E-mail: ajewett{at}ucla.edu.

Down-modulation of CD16 (FcRIII) receptors and loss of natural killer (NK) cell function have been observed in oral cancer patients. However, neither the mechanisms nor the significance of the decrease in CD16 receptors have been fully understood. The cytotoxic activity and survival of NK cells are negatively regulated by antibodies directed against CD16 surface receptor. The addition of anti-CD94 antibody in combination with either F(ab')₂ fragment or intact anti-CD16 antibody to NK cells resulted in significant inhibition of NK cell cytotoxic function and induction of apoptosis in resting human peripheral blood NK cells. Addition of interleukin-2 to anti-CD16 and/or anti-CD94 antibody-treated NK cells significantly inhibited apoptosis and increased the function of NK cells. There was a significant increase in tumor necrosis factor- (TNF-) but not IFN- secretion in NK cells treated either with anti-CD16 antibody alone or in combination with anti-CD94 antibodies. Consequently, the addition of anti-TNF- antibody partially inhibited apoptosis of NK cells mediated by the combination of anti-CD94 and anti-CD16 antibodies. Increase in apoptotic death of NK cells also correlated with an increase in type 2 inflammatory cytokines and in the induction of chemokines. Thus, we conclude that binding of antibodies to CD16 and CD94 NK cell receptors induces death of the NK cells and signals for the release of chemokines.

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				A. Jewett, C. Head, and N.A. Cacalano Emerging Mechanisms of Immunosuppression in Oral Cancers. J. Dent. Res., December 1, 2006; 85(12): 1061 - 1073. [Abstract] [Full Text] [PDF]