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 1
NKT cells constitutively express surface FcγRIII. (A) FcγRI, -II, -III, and -IV expression on sorted NK1.1⁺TCRβ⁺ NKT cells, NK1.1⁺TCRβ^– NK cells, and splenocytes (SPC) freshly isolated from B6 mice was analyzed by RT-PCR. (B) FcγRII and FcγRIII expression was analyzed on gated NKT cells, NK cells, NK1.1^–TCRβ⁺ T cells, and B220⁺ B cells using 2.4G2 or Ly17.2 mAb. Cells were also preincubated with Ly17.2 mAb and stained with 2.4G2. As a negative control, cells were stained with isotype-matched IgG for 2.4G2 or Ly17.2 mAbs (open histogram). Numbers indicate mean fluorescence intensity (MFI) ± SD. (C) The expression of CD4/CD8 or Vα14⁺TCR was analyzed on gated TCRβ⁺2.4G2⁺ liver MNCs using anti-CD4 and CD8 mAb or α-GalCer/CD1d dimer. Numbers indicate percent of cells ± SD. (D) Liver MNCs were freshly isolated from B6 mice and cultured with α-GalCer (220 ng/ml) or aggregated IgG (Agg IgG; 10 μg/ml) for 24 hours. FcγRIII expression was analyzed on gated NKT, NK, and T cells. Open histograms represent negative controls, which were stained with anti-NK1.1 and -TCRβ mAbs and isotype-matched IgG for 2.4G2. Numbers indicate MFI ± SD. Results are representative of 3 independent experiments. *P < 0.05.