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Association with FcRgamma is essential for activation signal through NKR-P1 (CD161) in natural killer (NK) cells and NK1.1+ T cells.

Arase N, Arase H, Park SY, Ohno H, Ra C, Saito T - J. Exp. Med. (1997)

Bottom Line: In this study, we analyzed the cell surface complex associated with NKR-P1 on NK cells and found that NKR-P1 associates with the FcRgamma chain which is an essential component of Fc receptors for IgG and IgE.Similarly, NK1.1+ T cells from FcRgamma-deficient mice did not produce IFN-gamma upon NKR-P1 crosslinking.These findings demonstrate that the FcRgamma chain plays an important role in activation of NK cells via the NKR-P1 molecule.

View Article: PubMed Central - PubMed

Affiliation: Division of Molecular Genetics, Center for Biological Science, Chiba University School of Medicine, Chiba 260, Japan.

ABSTRACT
Natural killer (NK) cells exhibit cytotoxicity against variety of tumor cells and virus-infected cells without prior sensitization and represent unique lymphocytes involved in primary host defense. NKR-P1 is thought to be one of NK receptors mediating activation signals because cross-linking of NKR-P1 activates NK cells to exhibit cytotoxicity and IFN-gamma production. However, molecular mechanism of NK cell activation via NKR-P1 is not well elucidated. In this study, we analyzed the cell surface complex associated with NKR-P1 on NK cells and found that NKR-P1 associates with the FcRgamma chain which is an essential component of Fc receptors for IgG and IgE. The association between FcRgamma and NKR-P1 is independent of Fc receptor complexes. Furthermore, NK cells from FcRgamma-deficient mice did not show cytotoxicity or IFN-gamma production upon NKR-P1 cross-linking. Similarly, NK1.1+ T cells from FcRgamma-deficient mice did not produce IFN-gamma upon NKR-P1 crosslinking. These findings demonstrate that the FcRgamma chain plays an important role in activation of NK cells via the NKR-P1 molecule.

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Defect of NK1.1  mediated cytotoxicity by NK  cells from γ−/− mice. Cytotoxicity of NK cells from γ+/+, γ+/−,  and γ−/− mice against P815 cell  line was analyzed in the presence  (open circles) or absence (closed circles) of anti-NK1.1 mAb. Data  are presented as mean ± SD of  triplicate assay.
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Figure 6: Defect of NK1.1 mediated cytotoxicity by NK cells from γ−/− mice. Cytotoxicity of NK cells from γ+/+, γ+/−, and γ−/− mice against P815 cell line was analyzed in the presence (open circles) or absence (closed circles) of anti-NK1.1 mAb. Data are presented as mean ± SD of triplicate assay.

Mentions: We also investigated the involvement of FcRγ in the NKR-P1–mediated cytotoxicity of NK cells. Since NKR-P1 is known to induce redirected cytotoxicity against FcR-expressing cells, we analyzed cytotoxicity of NK cells against FcR-expressing P815 cells in the presence of anti-NK1.1 mAb (Fig. 6). NK cells from γ+/+ and γ+/− mice showed increased cytotoxicity against P815 cells in the presence of anti-NK1.1 mAb, whereas NK cells from γ−/− mice failed to enhance cytotoxicity. These results demonstrate that FcRγ is involved in both IFN-γ production and cytotoxicity upon stimulation through the NKR-P1 molecule.


Association with FcRgamma is essential for activation signal through NKR-P1 (CD161) in natural killer (NK) cells and NK1.1+ T cells.

Arase N, Arase H, Park SY, Ohno H, Ra C, Saito T - J. Exp. Med. (1997)

Defect of NK1.1  mediated cytotoxicity by NK  cells from γ−/− mice. Cytotoxicity of NK cells from γ+/+, γ+/−,  and γ−/− mice against P815 cell  line was analyzed in the presence  (open circles) or absence (closed circles) of anti-NK1.1 mAb. Data  are presented as mean ± SD of  triplicate assay.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2199168&req=5

Figure 6: Defect of NK1.1 mediated cytotoxicity by NK cells from γ−/− mice. Cytotoxicity of NK cells from γ+/+, γ+/−, and γ−/− mice against P815 cell line was analyzed in the presence (open circles) or absence (closed circles) of anti-NK1.1 mAb. Data are presented as mean ± SD of triplicate assay.
Mentions: We also investigated the involvement of FcRγ in the NKR-P1–mediated cytotoxicity of NK cells. Since NKR-P1 is known to induce redirected cytotoxicity against FcR-expressing cells, we analyzed cytotoxicity of NK cells against FcR-expressing P815 cells in the presence of anti-NK1.1 mAb (Fig. 6). NK cells from γ+/+ and γ+/− mice showed increased cytotoxicity against P815 cells in the presence of anti-NK1.1 mAb, whereas NK cells from γ−/− mice failed to enhance cytotoxicity. These results demonstrate that FcRγ is involved in both IFN-γ production and cytotoxicity upon stimulation through the NKR-P1 molecule.

Bottom Line: In this study, we analyzed the cell surface complex associated with NKR-P1 on NK cells and found that NKR-P1 associates with the FcRgamma chain which is an essential component of Fc receptors for IgG and IgE.Similarly, NK1.1+ T cells from FcRgamma-deficient mice did not produce IFN-gamma upon NKR-P1 crosslinking.These findings demonstrate that the FcRgamma chain plays an important role in activation of NK cells via the NKR-P1 molecule.

View Article: PubMed Central - PubMed

Affiliation: Division of Molecular Genetics, Center for Biological Science, Chiba University School of Medicine, Chiba 260, Japan.

ABSTRACT
Natural killer (NK) cells exhibit cytotoxicity against variety of tumor cells and virus-infected cells without prior sensitization and represent unique lymphocytes involved in primary host defense. NKR-P1 is thought to be one of NK receptors mediating activation signals because cross-linking of NKR-P1 activates NK cells to exhibit cytotoxicity and IFN-gamma production. However, molecular mechanism of NK cell activation via NKR-P1 is not well elucidated. In this study, we analyzed the cell surface complex associated with NKR-P1 on NK cells and found that NKR-P1 associates with the FcRgamma chain which is an essential component of Fc receptors for IgG and IgE. The association between FcRgamma and NKR-P1 is independent of Fc receptor complexes. Furthermore, NK cells from FcRgamma-deficient mice did not show cytotoxicity or IFN-gamma production upon NKR-P1 cross-linking. Similarly, NK1.1+ T cells from FcRgamma-deficient mice did not produce IFN-gamma upon NKR-P1 crosslinking. These findings demonstrate that the FcRgamma chain plays an important role in activation of NK cells via the NKR-P1 molecule.

Show MeSH
Related in: MedlinePlus