FcγRIII engagement provides activating signals to NKT cells in antibody-induced joint inflammation
J. Clin. Invest. Hye Young Kim, et al. 116:2484 doi:10.1172/JCI27219 [Go to this article.]

Figure 4
Fc γR -deficient NKT cells are activated by α-GalCer. (A) Liver MNCs were freshly isolated from B6 or FcγR^–/– mice and analyzed for NKT cells by examining NK1.1 and TCRβ expression using flow cytometry. The numbers of NK, NKT, CD4⁺, and CD8⁺ cells were also counted. (B) Liver MNCs were freshly isolated from B6 or FcγR^–/– mice and cultured with α-GalCer (220 ng/ml) for 48 hours. The amounts of IL-4, IFN-γ, IL-10, and IL-13 in the culture supernatants were measured using ELISA. (C) B6 and FcγR^–/– mice were injected i.p. with α-GalCer (1 μg in 300 μl PBS). Serum IL-4, IFN-γ, IL-10, and IL-13 levels were monitored using ELISA 12 hours after α-GalCer injection. Data are mean ± SD for 3 mice per group. Similar results were obtained from 3 independent experiments.