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IgE-Mediated Activation of NK Cells Through FcRIII¹

Noriko Arase^*,, Hisashi Arase^*, Satoshi Hirano^*, Tadashi Yokosuka^*, Daiju Sakurai^* and Takashi Saito^2,*,

^* Department of Molecular Genetics, Graduate School of Medicine, Chiba University, Chiba, Japan; and Laboratory of Cell Signaling, RIKEN, Research Center for Allergy and Immunology, Yokohama, Kanagawa, Japan

NK cells express FcRIII (CD16), which is responsible for IgG-dependent cell cytotoxicity and for production of several cytokines and chemokines. Whereas FcRIII on NK cells is composed of both FcRIII and FcR chains, that on mast cells is distinct from NK cells and made of FcRIII, FcR, and FcR. Mast cells show degranulation and release several mediators, which cause anaphylactic responses upon cross-linking of FcRIII as well as FcRI with aggregated IgE. In this paper, we examined whether IgE activates NK cells through FcRIII on their cell surface. We found that NK cells produce several cytokines and chemokines related to an allergic reaction upon IgE stimulation. Furthermore, NK cells exhibited cytotoxicity against IgE-coated target cells in an FcRIII-dependent manner. These effects of IgE through FcRIII were not observed in NK cells from FcR-deficient mice lacking FcRIII expression. Collectively, these results demonstrate that NK cells can be activated with IgE through FcRIII and exhibit both cytokine/chemokine production and Ab-dependent cell cytotoxicity. These data imply that not only mast cells but also NK cells may contribute to IgE-mediated allergic responses.

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