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Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan;
CREST (Core Research for Evolutional Science and Technology) of Japan Science and Technology Corp., Chiyoda-ku, Tokyo, Japan;
Department of First Surgery, Faculty of Medicine, University of Tokyo, Tokyo, Japan;
§
Department of Pathogenic Biochemistry, Research Institute of Wakan-yaku, Toyama Medical and Pharmaceutical University, Toyama, Japan; and
¶
Central Institute for Experimental Animals, Nogawa, Miyamae, Kawasaki, Japan
CD27, a member of the TNF receptor superfamily, has been implicated
in T cell activation, T cell development, and T cell-dependent Ab
production by B cells. In the present study we examined the expression
and function of CD27 on murine NK cells. Murine NK cells constitutively
expressed CD27 on their surface. Stimulation with immobilized
anti-CD27 mAb or murine CD27 ligand (CD70) transfectans solely
could induce proliferation and IFN-
production of freshly isolated
NK cells and enhanced the proliferation and IFN-
production of
anti-NK1.1-sutimulated NK cells. Although NK cell cytotoxicity was
not triggered by anti-CD27 mAb or against CD70 transfectants,
prestimulation via CD27 enhanced the cytotoxic activity of NK cells in
an IFN-
-dependent manner. These results suggest that CD27-mediated
activation may be involved in the NK cell-mediated innate immunity
against virus-infected or transformed cells expressing
CD70.
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