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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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Related in: MedlinePlus

Defect of IFN-γ production by  NK1.1+ T cells from γ−/− mice upon stimulation with NK1.1 cross-linking. NK1.1+  T cells from γ+/+ (closed bar) and γ−/− (open  bar) mice were stimulated with immobilized  anti-NK1.1 mAb or anti-TCRβ mAb and  IFN-γ and IL-4 produced in the culture supernatant was measured. Data are presented  as mean ± SD of triplicate culture.
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Figure 5: Defect of IFN-γ production by NK1.1+ T cells from γ−/− mice upon stimulation with NK1.1 cross-linking. NK1.1+ T cells from γ+/+ (closed bar) and γ−/− (open bar) mice were stimulated with immobilized anti-NK1.1 mAb or anti-TCRβ mAb and IFN-γ and IL-4 produced in the culture supernatant was measured. Data are presented as mean ± SD of triplicate culture.

Mentions: Because NK1.1+ T cells also produce IFN-γ but not IL-4 upon NKR-P1 cross-linking (10), we also analyzed the function of NK1.1+ T cells in γ−/− mice. As we have previously reported (22), NK1.1+ T cells develop normally in γ−/− mice. NK1.1+ T cells were prepared from γ+/+ and γ−/− mice and stimulated with immobilized anti-NK1.1 mAb (Fig. 5). Similar to NK cells, NK1.1+ T cells from γ−/− mice did not produce IFN-γ upon NKR-P1 cross-linking whereas these cells from γ+/+ mice produced a significant amount of IFN-γ. In contrast to the stimulation through NKR-P1, NK1.1+ T cells from both γ+/+ and γ−/− mice produced IFN-γ and IL-4 upon TCR crosslinking. These observations demonstrate that the FcRγ chain is required for IFN-γ production via NKR-P1 cross-linking both in NK cells and NK1.1+ T cells.


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 IFN-γ production by  NK1.1+ T cells from γ−/− mice upon stimulation with NK1.1 cross-linking. NK1.1+  T cells from γ+/+ (closed bar) and γ−/− (open  bar) mice were stimulated with immobilized  anti-NK1.1 mAb or anti-TCRβ mAb and  IFN-γ and IL-4 produced in the culture supernatant was measured. Data are presented  as mean ± SD of triplicate culture.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 5: Defect of IFN-γ production by NK1.1+ T cells from γ−/− mice upon stimulation with NK1.1 cross-linking. NK1.1+ T cells from γ+/+ (closed bar) and γ−/− (open bar) mice were stimulated with immobilized anti-NK1.1 mAb or anti-TCRβ mAb and IFN-γ and IL-4 produced in the culture supernatant was measured. Data are presented as mean ± SD of triplicate culture.
Mentions: Because NK1.1+ T cells also produce IFN-γ but not IL-4 upon NKR-P1 cross-linking (10), we also analyzed the function of NK1.1+ T cells in γ−/− mice. As we have previously reported (22), NK1.1+ T cells develop normally in γ−/− mice. NK1.1+ T cells were prepared from γ+/+ and γ−/− mice and stimulated with immobilized anti-NK1.1 mAb (Fig. 5). Similar to NK cells, NK1.1+ T cells from γ−/− mice did not produce IFN-γ upon NKR-P1 cross-linking whereas these cells from γ+/+ mice produced a significant amount of IFN-γ. In contrast to the stimulation through NKR-P1, NK1.1+ T cells from both γ+/+ and γ−/− mice produced IFN-γ and IL-4 upon TCR crosslinking. These observations demonstrate that the FcRγ chain is required for IFN-γ production via NKR-P1 cross-linking both in NK cells and NK1.1+ T cells.

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