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• W1570697608 abstract "Abstract IL-12 is a potent proinflammatory cytokine. The effects of IL-12 are thought to be mediated by IFN-γ production by NK, NKT, and T cells. In this study, we show that although IL-12 stimulates NK and NK1.1+ T cells in bulk mouse splenocytes, it does not significantly stimulate purified NK cells, indicating that other cells are required. IL-12 stimulates T cell-deficient spleen cells and those depleted of macrophages. Unexpectedly, the depletion of dendritic cells also has little effect on the stimulation of spleen cells with IL-12. In contrast, B cell depletion almost completely inhibits IL-12-induced IFN-γ production and B cell-deficient spleen cells are poorly stimulated with IL-12. Furthermore, purified NK cells are stimulated with IL-12 in the presence of purified B cells. Thus, B cells are necessary and also sufficient for the stimulation of purified NK cells with IL-12. Whereas spleen cells from IL-18-deficient mice are not stimulated with IL-12, NK cells purified from IL-18-deficient mice are stimulated with IL-12 in the presence of wild-type (WT) B cells, and WT NK cells are not stimulated with IL-12 in the presence of IL-18-deficient B cells. Cell contact between B and NK cells is also required for IL-12-induced IFN-γ production. Finally, B cell-deficient mice injected with IL-12 produce significantly less IFN-γ and IL-18 in the sera than WT mice do. Thus, stimulation of NK cells with IL-12 requires B cell cooperation in vitro as well as in vivo." @default.
• W1570697608 created "2016-06-24" @default.
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• W1570697608 date "2009-09-15" @default.
• W1570697608 modified "2023-09-27" @default.
• W1570697608 title "An Accessory Role for B Cells in the IL-12-Induced Activation of Resting Mouse NK Cells" @default.
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• W1570697608 doi "https://doi.org/10.4049/jimmunol.0901391" @default.
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